The genetic architecture of neurodevelopmental disorders (NDD) and autism spectrum disorder (ASD) spans synaptic scaffolding and neurotransmission, chromatin remodeling and epigenetic regulation, transcriptional and translational control, ion channel and receptor function, cytoskeletal and cell-adhesion pathways, and key neurodevelopmental signaling cascades (including mTOR and RAS–MAPK). Germline disruption across these pathways underlies a wide spectrum of clinical presentations, including global developmental delay, intellectual disability, speech and language impairment, autism spectrum features and social communication deficits, epilepsy and epileptic encephalopathy, movement and tone abnormalities, microcephaly or macrocephaly, congenital brain malformations, and complex behavioral or psychiatric phenotypes. Many affected individuals also have multisystem involvement (e.g., congenital anomalies, growth abnormalities, cardiac or endocrine features), making purely clinical localization challenging. Early, accurate molecular diagnosis is essential for clarifying etiology, informing prognosis, identifying targeted treatment or syndrome-specific surveillance where available, and connecting patients and families to appropriate resources and clinical trials.
PreCheck Health Services’ Neurodevelopmental & Autism Spectrum Disorders Panel is an advanced targeted exome assay encompassing genes implicated in monogenic forms of NDD and ASD, syndromic and non-syndromic intellectual disability, epileptic encephalopathies, congenital brain malformations, and recognizable neurogenetic syndromes with prominent developmental and behavioral manifestations. The panel is curated using evidence from ACMG, ClinGen, OMIM, GeneReviews, and current peer-reviewed literature to prioritize genes with well-established gene–disease relationships and clinically actionable or management-informing phenotypes. This approach enables identification of meaningful germline variants that support definitive diagnosis, refine etiologic classification, guide neurologic and developmental management (including seizure and behavioral treatment strategies and syndrome-specific monitoring such as tumor, cardiac, or ophthalmologic surveillance), and facilitate cascade testing, reproductive counseling, and long-term care planning for affected families.
This assay is designed for patients presenting with or at risk for:
• Global developmental delay or intellectual disability of unknown etiology, particularly when accompanied by dysmorphic features, congenital anomalies, or growth abnormalities
• Autism spectrum disorder, social communication disorder, or prominent autistic traits with or without intellectual disability, especially when there is a family history of NDD/ASD or other neuropsychiatric conditions
• Unexplained speech and language delay, apraxia of speech, or severe expressive/receptive language impairment
• Epilepsy or epileptic encephalopathy (e.g., infantile spasms, early-onset refractory seizures, developmental and epileptic encephalopathies) where a monogenic cause is suspected
• Abnormal brain MRI or neuroimaging findings (e.g., malformations of cortical development, corpus callosum abnormalities, cerebellar hypoplasia, white matter changes) suggesting a genetic neurodevelopmental disorder
• Microcephaly, macrocephaly, or significant head circumference outliers, particularly when associated with developmental delay, seizures, or autism spectrum features
• Syndromic presentations with combined developmental, behavioral, and systemic features (e.g., cardiac, renal, endocrine, ophthalmologic, or dermatologic findings) in which a recognizable or suspected neurogenetic syndrome is in the differential diagnosis
• Individuals with a personal or family history of confirmed or suspected monogenic neurodevelopmental or autism spectrum disorder in whom the specific molecular diagnosis remains unresolved, or where clarifying carrier status and recurrence risk is important for reproductive planning and cascade testing
This Neurodevelopmental & Autism Spectrum Disorders Panel encompasses genes central to synaptic transmission, ion channel and receptor function, chromatin remodeling and epigenetic control, transcriptional regulation of brain development, RNA processing and cohesin-mediated gene regulation, cytoskeletal architecture and neuronal migration, and glycosylation/metabolic pathways with major neurodevelopmental impact. Genes are organized into biologic and clinical pathways relevant to global developmental delay, intellectual disability, autism spectrum disorder, epileptic encephalopathy, congenital brain malformations, and multisystem neurogenetic syndromes.
1.Synaptic Transmission, Ion Channels, and Epileptic Encephalopathy
Genes encoding ligand- and voltage-gated receptors, ion channels, synaptic vesicle proteins, and key signaling molecules governing excitatory and inhibitory neurotransmission. Pathogenic variants are associated with epilepsy and developmental and epileptic encephalopathies, ASD with seizures, and cognitive/behavioral phenotypes driven by synaptic dysfunction. Representative genes include:
• CACNA1A, CACNA1D, CACNA1E, CACNA2D2, CAMK2A, GABRA1, GABRB2, GABRB3, GABRG2, GRIA2, GRIA3, GRIA4, GRIK2, GRIN1, GRIN2A, GRIN2B, ITPR1, KCNB1, KCNC2, KCNH1, KCNH5, KCNQ2, KCNQ3, KCNT1, SCN1A, SCN2A, SCN3A, SCN8A, SLC2A1, SLC6A8, SLC9A6, SLC16A2, SNAP25, STX1B, STXBP1, SYN1, SYNGAP1, SYP, GPHN
2.Chromatin Remodeling, Epigenetic Regulation, and Histone Modification
Genes encoding components of SWI/SNF and related chromatin-remodeling complexes, histone methyltransferases/demethylases, acetyltransferases, and other epigenetic regulators. Variants in these loci underline many syndromic intellectual disability and NDD/ASD phenotypes with characteristic dysmorphisms, growth abnormalities, and multisystem involvement. Representative genes include:
• ARID1A, ARID1B, ARID2, ASH1L, ASXL1, ASXL2, ASXL3, BPTF, BRD4, BRPF1, CHD1, CHD3, CHD4, CHD7, CHD8, CREBBP, CSNK2A1, CTCF, DNMT3A, DPF2, EHMT1, EED, EZH2, FBXO11, HDAC8, JARID2, KAT6A, KAT6B, KDM3B, KDM5B, KDM5C, KDM6B, KMT2B, KMT2C, KMT2D, KMT2E, MBD5, MECP2, NSD1, NSD2, NSUN2, PHF6, PHF8, PHF12, PHF21A, SET, SETBP1, SETD1B, SETD2, SETD5, SIN3A, TRRAP, YY1, ZEB2, ZNF292
3.Neurodevelopmental Transcription Factors, Signaling Pathways, and Brain Patterning Genes encoding transcription factors and signaling regulators that control neuronal differentiation, cortical lamination, regional patterning, and activity-dependent gene expression. Defects are associated with global developmental delay, intellectual disability, autism, language impairment, and distinctive neurobehavioral or structural brain phenotypes. Representative genes include:
• ADNP, BCL11A, BCL11B, CAMTA1, FOXP1, FOXP2, HOXA1, MEF2C, MEIS2, NFIB, NR2F1, NR4A2, POU3F3, PTEN, RAC1, RALA, RAI1, RELN, RERE, RFX3, RFX7, SATB1, SATB2, SCN related TF targets, SMAD4, SOX3, SOX5, SOX6, TBR1, TCF4, TCF7L2, TELO2, TRAF7, TRIO, WAC, WDFY3, ZBTB18, ZBTB20, ZMIZ1
4.Synaptic Scaffolding, Cell Adhesion, and Neuronal Connectivity
Genes encoding postsynaptic scaffolding proteins, neurexin–neuroligin complexes, cell adhesion molecules, and regulators of dendritic spine structure and synaptic stability. Variants in these genes are strongly enriched in ASD, intellectual disability, and NDD with prominent social-communication and behavioral phenotypes. Representative genes include:
• ANK2, ANK3, AUTS2, CASK, CC2D1A, CDKL5, DLG3, DLG4, FLNA, FRMPD4, L1CAM, MAGEL2, NBEA, NCKAP1, NLGN3, NLGN4X, NRXN1, OPHN1, PACS1, PACS2, PAFAH1B1, PLP1, RAB39B, SHANK1, SHANK2, SHANK3, SPTAN1, STX1B, STXBP1, SYN1, SYNGAP1, SYP, TANC2, TSPAN7, UBE3A, WDFY3, WWOX
5.RNA Processing, Cohesin Complex, and Global Gene Expression Machinery
Genes involved in mRNA processing, splicing, transport, nonsense-mediated decay, and dosage-sensitive regulation of large gene networks, including cohesin and related chromatin structural complexes. Pathogenic variants cause broad neurodevelopmental syndromes (e.g., Cornelia de Lange–spectrum, X-linked ID) with
multi-domain cognitive, behavioral, and physical manifestations. Representative genes include:
• AP1G1, AP1S2, AP4B1, AP4E1, AP4M1, AP4S1, BCAP31, CNOT1, CNOT3, CSDE1, DDX3X, DHX30, EFTUD2, HNRNPH2, HNRNPK, HNRNPR, HNRNPU, IQSEC2, NIPBL, RAD21, SMC1A, SRCAP, RPL10, RPS6KA3, SCAF4, STAG1, TELO2, THOC2, TNRC6B, UBTF, UPF3B, WDR26, WDR45, ZC4H2, ZDHHC9
6.Cytoskeletal Dynamics, Neuronal Migration, and Brain Malformations
Genes encoding microtubule components, actin-binding proteins, motor proteins, and regulators of mitotic spindle function and centrosomal integrity. Variants are associated with lissencephaly and other malformations of cortical development, microcephaly, hydrocephalus, and white matter/callosal abnormalities. Representative genes include:
• DCX, FLNA, HEPACAM, KIF1A, MCPH1, MID1, PAFAH1B1, SPTAN1, TUBA1A, TUBB2B, TUBB3, LINS1, MAGT1, NHS, NDE-related interactors (e.g., TRIO), TUSC3
7.Metabolic, Organelle, and Glycosylation-Related Neurodevelopmental Disorders Genes affecting peroxisomal and lysosomal function, sterol and lipid metabolism, folate and creatine pathways, copper and metal handling, glycosylation and GPI-anchor biosynthesis, and other metabolic processes that present with neurodevelopmental phenotypes. Representative genes include:
• ABCD1, ACSL4, ADSL, ALDH5A1, ALG1, ALG3, ALG6, ALG12, ATP6AP2, ATP7A, ATP13A2, DDOST, DHCR7, DKC1, EBP, FOLR1, GAMT, GATM, GK, HPRT1, IDS, MAOA, MAN1B1, MBOAT7, MBTPS2, MAGT1, NSDHL, OCRL, PGAP3, PIGL, PIGN, PLP1, PORCN, PSMD12, SER like proteostasis genes (e.g., UBE2A, USP7, USP9X), SMS, SLC2A1, SLC6A8, SLC9A6, SLC16A2, VPS13B, WWOX
Genes Analyzed 338 Neurodevelopment related genes.
Technology Platform Illumina NGS (Hybrid-Capture Target Enrichment).
Coverage Metrics >98% bases at ≥20× read depth.
Variant Types Detected SNVs and small indels (≤20 bp) within coding exons ±10 bp intronic boundaries.
Reference Genome GRCh38/hg38.
Bioinformatics Pipeline SeqOne™, ACMG/AMP compliant.
Confirmatory Testing Sanger sequencing or orthogonal method as indicated.
Turnaround Time ~10 calendar days.
Quality Metrics Read quality ≥Q30; allelic balance ≥0.3; minimum coverage 20×.
1.Congenital and Early-Onset Neurodevelopmental Disorders
❖ Clarify the etiology of global developmental delay and intellectual disability in infants and children, particularly when accompanied by dysmorphic features, congenital anomalies, or abnormal growth
❖ Distinguish isolated NDD from syndromic or multisystem disorders with important extracranial implications
❖ Support earlier diagnosis, prognostic counseling, and timely referral to appropriate development,
educational, and subspecialty services
2.Autism Spectrum Disorder, Communication, and Behavioral Phenotypes
❖ Identify genetic causes of autism spectrum disorder, social communication disorder, and complex behavioral phenotypes, including those with overlapping anxiety, ADHD, or mood symptoms
❖ Differentiate idiopathic ASD from recognizable neurogenetic syndromes where additional organ specific surveillance or targeted interventions may be required
❖ Inform individualized management plans, including behavioral therapies, educational support, and
consideration of syndrome-specific risks
3.Epilepsy, Developmental and Epileptic Encephalopathy, and Regression
❖ Define molecular causes of early-onset, refractory, or syndromic epilepsy and developmental and epileptic encephalopathies (DEE)
❖ Guide antiepileptic drug selection or avoidance (e.g., sodium channel disorders, mTORopathies), consideration of dietary therapies, and evaluation for targeted or emerging precision treatments
❖ Provide etiologic clarity in patients with developmental regression or plateauing, helping distinguish primary neurodegenerative disease from static injury or non-neurologic causes
4.Structural Brain Abnormalities, Microcephaly, and Macrocephaly
❖ Diagnose genetic causes of malformations of cortical development, midline and callosal anomalies, cerebellar and posterior fossa malformations, and other MRI-defined structural brain abnormalities
❖ Clarify the molecular basis of microcephaly or macrocephaly associated with NDD/ASD, epilepsy, or movement disorders, refining prognosis, and surveillance strategies
❖ Inform anticipatory guidance regarding motor, cognitive, and functional outcomes and the need for
targeted imaging or subspecialty follow-up
5.Multisystem Neurogenetic Syndromes, Family Management, and Cascade Testing
❖ Recognize chromatin, cohesin, metabolic, and other multisystem syndromes where neurodevelopmental disability and autism are central features of a broader phenotype
❖ Enable targeted cascade testing of relatives once a pathogenic or likely pathogenic variant is identified, clarifying carrier status, recurrence risk, and the need for developmental, neurologic, or systems-based surveillance in at-risk family members
❖ Integrate germline results with neuroimaging, EEG, clinical examination, and educational/behavioral
assessments to build durable, gene-informed care plans that coordinate pediatric and adult neurology,
medical genetics, psychiatry, developmental pediatrics, and primary care over the patient’s lifespan
Neurodevelopmental & Autism Spectrum Disorders testing provides clinically actionable information across medical genetics, child neurology, developmental pediatrics, psychiatry, psychology, clinical neurophysiology, and primary care, directly influencing diagnosis, risk assessment, surveillance, and treatment strategies.
Risk Stratification and Diagnostic Clarification
Identify pathogenic or likely pathogenic variants underlying global developmental delay and intellectual disability, autism spectrum disorder and related social communication disorders, developmental and epileptic encephalopathies, structural brain malformations, microcephaly, and macrocephaly, and chromatin/cohesin and metabolic neurogenetic syndromes. Distinguish primary genetic NDD/ASD from acquired or secondary etiologies (e.g., perinatal insult, environmental exposure, psychosocial factors), refine differential diagnoses generated by neuroimaging, EEG, and neuropsychological testing, and convert “probable” or “suspected” neurodevelopmental disorder into a definitive, gene-based diagnosis.
Family Risk Assessment, Cascade Testing, and Reproductive Counseling
Clarify recurrence risk for families and identify at-risk relatives once a familial variant is known, including siblings, future pregnancies, and extended family members with neurodevelopmental or psychiatric histories. Enable early surveillance and anticipatory guidance in gene-positive but minimally affected or presymptomatic individuals (e.g., targeted developmental monitoring, seizure vigilance, syndrome-specific organ screening), and inform reproductive planning, including options such as carrier testing, prenatal diagnosis, and preimplantation genetic testing when appropriate.
Treatment Selection, Supportive Planning, and Therapeutic Optimization
Use genotype to inform selection or avoidance of specific antiseizure medications, consideration of dietary or targeted therapies (e.g., GLUT1 deficiency, creatine deficiency, certain metabolic or mTOR-related disorders), and prioritization of syndrome-specific interventions (e.g., PTEN-related cancer screening, TSC-related surveillance, management of sleep, behavioral, or psychiatric comorbidities). Guide intensity and focus of behavioral, educational, and psychosocial supports, set realistic expectations for developmental trajectories, and identify eligibility for clinical trials and emerging gene- or pathway-directed therapies.
Integrated Longitudinal Neurodevelopmental Care
Support multidisciplinary teams (medical genetics, neurology, developmental pediatrics, psychiatry, psychology, physical/occupational/speech therapy, education specialists, and primary care) in building unified, gene-informed care plans that coordinate developmental services, seizure and behavior management, neuroimaging and EEG follow-up, and screening for associated systemic complications across the lifespan. Provide a durable framework for adapting management as guidelines, therapies, and variant classifications evolve, and for managing complex hereditary neurodevelopmental and autism spectrum conditions within affected families through coordinated pediatric-to-adult transition and ongoing cascade testing.
This Neurodevelopmental Disorders & Autism Spectrum Panel is best used as part of a multi-dimensional diagnostic strategy, often in combination with:
Pharmacogenetics Testing (for drug metabolism and gene-drug interactions)
Together, these tools enable precision medicine teams to offer a fully customized, data-driven treatment plan for each patient.
Germline testing for neurodevelopmental and autism spectrum disorders is now a critical component of precision care, allowing clinicians to define the molecular basis of global developmental delay and intellectual disability, autism spectrum and social communication disorders, developmental and epileptic encephalopathies, structural brain malformations, microcephaly and macrocephaly, and chromatin/cohesin and metabolic neurogenetic syndromes with far greater resolution than clinical, imaging, and neuropsychological assessment alone. With a rigorously curated gene panel, high analytic performance, and clinically validated interpretation, PreCheck Health Services provides the genomic insights necessary to refine diagnosis, clarify prognosis, guide seizure, and behavioral management, inform syndrome-specific surveillance, and support cascade testing and reproductive counseling. This integrated approach enables earlier, more precise, and more preventive management across the full spectrum of hereditary and familial neurodevelopmental and autism spectrum conditions, improving outcomes for affected patients and at-risk relatives.
The Neurodevelopmental Disorders & Autism Spectrum Panel is designed to detect single-nucleotide variants (SNVs) and small insertions and deletions in 338 genes associated with neurodevelopmental disorders. Targeted regions for this panel include the coding exons and 10 bp intronic sequences immediately to the exon intron boundary of each coding exon in each of these genes. Extracted patient DNA is prepared using targeted hybrid capture, assignment of a unique index, and sequencing via Illumina sequencing by synthesis (SBS) technology. Data is aligned using the human genome build GRCh38. Variant interpretation is performed according to current American College of Medical Genetics and Genomics (ACMG) professional guidelines for the interpretation of germline sequence variants using SeqOne Pipeline.
ABCD1, ACSL4, ADNP, ADSL, AFF2, AHDC1, ALDH5A1, ALG1, ALG3, ALG6, ALG12, ANK2, ANK3, ANKRD11, ANKRD17, AP1G1, AP1S2, AP4B1, AP4E1, AP4M1, AP4S1, ARHGEF9, ARID1A, ARID1B, ARID2, ARX, ASH1L, ASXL1, ASXL2, ASXL3, ATP6AP2, ATP7A, ATP13A2, ATRX, AUTS2, BCAP31, BCL11A, BCL11B, BICRA, BPTF, BRD4, BRPF1, BRSK2, BRWD3, CA8, CACNA1A, CACNA1D, CACNA1E, CACNA2D2, CAMK2A, CAMTA1, CASK, CC2D1A, CCDC22, CDK13, CDKL5, CHAMP1, CHD1, CHD3, CHD4, CHD7, CHD8, CIC, CLCN4, CNKSR2, CNOT1, CNOT3, CRADD, CRBN, CREBBP, CSDE1, CSNK2A1, CTCF, CTNNB1, CTR9, CUL3, CUL4B, DCX, DDOST, DDX3X, DHCR7, DHX30, DKC1, DLG3, DLG4, DNM1, DNMT3A, DPF2, DYRK1A, EBF3, EBP, EED, EFTUD2, EHMT1, EIF2S3, EIF3F, EXOC7, EZH2, FBXO11, FGD1, FGF12, FLNA, FMR1, FOLR1, FOXP1, FOXP2, FRMPD4, FTSJ1, GABRA1, GABRB2, GABRB3, GABRG2, GAMT, GATAD2B, GATM, GDI1, GK, GNAI1, GNB1, GPC3, GPHN, GRIA1, GRIA2, GRIA3, GRIA4, GRIK2, GRIN1, GRIN2A, GRIN2B, HCFC1, HDAC8, HECW2, HEPACAM, HIVEP2, HNRNPH2, HNRNPK, HNRNPR, HNRNPU, HOXA1, HPRT1, HUWE1, IDS, IL1RAPL1, IQSEC2, ITPR1, JARID2, KANSL1, KAT6A, KAT6B, KCNB1, KCNC2, KCNH1, KCNH5, KCNQ2, KCNQ3, KCNT1, KDM3B, KDM5B, KDM5C, KDM6B, KIF1A, KMT2B, KMT2C, KMT2D, KMT2E, KPTN, L1CAM, LINS1, MAGEL2, MAGT1, MAN1B1, MAOA, MBD5, MBOAT7, MBTPS2, MCPH1, MECP2, MED12, MED13, MED13L, MED23, MEF2C, MEIS2, MID1, MSL3, MYT1L, NAA10, NAA15, NACC1, NBEA, NCKAP1, NDP, NEXMIF, NFIB, NHS, NIPBL, NLGN3, NLGN4X, NONO, NOVA2, NR2F1, NR4A2, NRXN1, NSD1, NSD2, NSDHL, NSUN2, OCRL, OFD1, OPHN1, OTUD6B, PACS1, PACS2, PAFAH1B1, PAK3, PGAP3, PHF6, PHF8, PHF12, PHF21A, PHIP, PIDD1, PIGL, PIGN, PLP1, POGZ, PORCN, POU3F3, PPM1D, PPP2R1A, PPP2R5D, PPP3CA, PQBP1, PRPS1, PSMD12, PTCHD1, PTEN, QRICH1, RAB39B, RAC1, RAD21, RAI1, RALA, RELN, RERE, RFX3, RFX7, RPL10, RPS6KA3, SATB1, SATB2, SCAF4, SCN1A, SCN2A, SCN3A, SCN8A, SET, SETBP1, SETD1B, SETD2, SETD5, SHANK1, SHANK2, SHANK3, SIN3A, SLC2A1, SLC6A8, SLC9A6, SLC16A2, SMAD4, SMARCA2, SMARCA4, SMARCA5, SMARCB1, SMARCC2, SMARCE1, SMC1A, SMS, SNAP25, SON, SOX3, SOX5, SOX6, SPTAN1, SRCAP, ST3GAL3, STAG1, STX1B, STXBP1, SYN1, SYNGAP1, SYP, TANC2, TAOK1, TBCK, TBL1XR1, TBR1, TCF4, TCF7L2, TELO2, TFE3, THOC2, TNRC6B, TRAF7, TRAPPC9, TRIM8, TRIO, TRIP12, TRPM3, TRRAP, TSPAN7, TUBA1A, TUBB2B, TUBB3, TUSC3, UBE2A, UBE3A, UBTF, UPF3B, USP7, USP9X, VPS13B, WAC, WDFY3, WDR26, WDR45, WWOX, YY1, ZBTB18, ZBTB20, ZC4H2, ZDHHC9, ZEB2, ZFX, ZMIZ1, ZNF292, ZNF711, H1-4
This test aims to detect all clinically relevant variants within the coding regions of the genes evaluated. Pathogenic and likely pathogenic variants detected in these genes should be confirmed by orthogonal methods. Detected genetic variants classified as benign, likely benign, or of uncertain significance are not included in this report. Homopolymer regions and regions outside of the coding regions cannot be captured by the standard NGS target enrichment protocols. Currently, the assay does not detect large deletions and duplications. This analysis also cannot detect pathogenic variants within regions that were not analyzed (e.g., introns, promoter and enhancer regions, long repeat regions, and mitochondrial sequence). This assay is not designed to detect mosaicism and is not designed to detect complex gene rearrangements or genomic aneuploidy events. It is important to understand that there may be variants in these genes undetectable using current technology. Additionally, there may be genes associated with neurodevelopmental disorders & autism pathology whose clinical association has not yet been definitively established. The test may therefore not detect all variants associated with neurodevelopmental disorders & autism. The interpretation of variants is based on our current understanding of the genes in this panel and is based on current ACMG professional guidelines for the interpretation of germline sequence variants. Interpretations may change over time as more information about the genes in this panel becomes available. Qualified health care providers should be aware that future reclassifications of genetic variants can occur as ACMG guidelines are updated. Factors influencing the quantity and quality of extracted DNA include, but are not limited to, collection technique, the amount of buccal epithelial cells obtained, the patient’s oral hygiene, and the presence of dietary or microbial sources of nucleic acids and nucleases, as well as other interfering substances and matrix-dependent influences. PCR inhibitors, extraneous DNA, and nucleic acid-degrading enzymes may adversely affect assay results.
This laboratory-developed test (LDT) was developed, and its performance characteristics were determined by PreCheck Health Services, Inc. This test was performed at PreCheck Health Services, Inc. (CLIA ID: 10D2210020 and CAP ID: 9101993), which is certified under the Clinical Laboratory Improvement Amendments of 1988 (CLIA) as qualified to perform high complexity testing.
This assay has not been cleared or approved by the U.S. Food and Drug Administration (FDA). Clearance or approval by the FDA is not required for the clinical use of this analytically and clinically validated laboratory developed test. This assay has been developed for clinical purposes, and should not be regarded as investigational or used for research.
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