NM_000314.8:c.1211G>T (p.Ter404LeuextTer8) is a stop-loss variant in PTEN that removes the native stop codon and extends the protein by 8 amino acids. The variant is absent from gnomAD v2.1, v4.1, and gnomAD-Canada, meeting PM2_Supporting under the PTEN VCEP v3.2.¹ The variant is absent from ClinVar. It has been reported in COSMIC (COSV64296267) in two somatic cancer samples, but no germline disease associations have been established.² No functional data is available for this stop-loss variant. The PTEN VCEP PVS1 decision tree does not cover stop-loss variants (limited to nonsense, frameshift, splice site, and exon deletions). The Mighell et al. 2018 phosphatase saturation mutagenesis assay evaluates missense substitutions only and does not include stop-loss variants.³ No de novo observations, segregation data, or case-control studies are available. No publications were identified that mention this specific variant.⁴ With only PM2_Supporting met (absent from population databases) and all other criteria either not met or not applicable, this variant does not reach any classification threshold under the PTEN VCEP v3.2 combination rules and remains a Variant of Uncertain Significance (VUS). Notably, PM4 (protein extension from stop-loss) is flagged for human review — the VCEP PM4 rule explicitly covers stop-loss variants causing protein extension, and if applied at Moderate strength, the combination of PM4 + PM2_Supporting could support Likely Pathogenic under certain rule configurations.⁵