NM_006180.4:c.1529C>A is a nonsense variant in NTRK2 predicting p.(Ser510Ter), meeting PVS1 at very strong strength under the ClinGen SVI PVS1 framework (PMC6185798). NTRK2 loss-of-function is an established mechanism for autosomal dominant obesity, hyperphagia, and developmental delay (MIM #613886). The premature termination codon in exon 16 of 20 is predicted to trigger nonsense-mediated decay.¹ The variant is absent from gnomAD v2.1, v4.1, and gnomAD-Canada population databases, meeting PM2 at moderate strength.² Applying generic ACMG/AMP 2015 combination rules (PMID:25741868): one Very Strong criterion (PVS1) plus one Moderate criterion (PM2) meets the threshold for Pathogenic classification.³ The pipeline-derived PVS1 gene-context literature search returned five supporting papers (PMIDs 42018264, 30717682, 32082673, 39112663, 39341363), but none of these papers mention NM_006180.4:c.1529C>A or provide evidence for NTRK2 germline loss-of-function as a disease mechanism. The gene-level PVS1 eligibility determination is independently supported by established OMIM curation (MIM #613886) rather than by the pipeline's literature search results.