NM_000264.5:c.1085C>T (p.Thr362Ile) is a missense variant in PTCH1, a gene in which heterozygous pathogenic variants cause Gorlin syndrome (nevoid basal cell carcinoma syndrome), an autosomal dominant tumor-predisposition disorder.¹ The variant is absent from all population databases queried: gnomAD v2.1, gnomAD v4.1, and gnomAD-Canada v1.0 (allele frequency 0.0% in all populations). This absence meets PM2 at supporting level.² REVEL in silico meta-predictor scores the variant as 0.809, predicting a damaging effect on protein function. BayesDel scores 0.454 (borderline). SpliceAI predicts no significant splicing impact (max delta = 0.11). These computational predictions meet PP3 at supporting level.³ The variant has been observed once in somatic cancers (COSMIC COSV59504254) but has not been reported in ClinVar as a germline variant, and no functional studies, de novo reports, segregation data, or case-control studies for this variant were identified in the literature.⁴ No other ACMG/AMP criteria are met. PVS1 is not applicable because this is a missense variant and SpliceAI does not predict a null effect. PS1-PS5, PM1, PM5, PM6, PP1-PP2, PP4-PP5, BA1, BS1-BS4, BP1-BP7 are either not met or not applicable. Applying the generic ACMG/AMP 2015 final combination rules (Richards et al. 2015, PMID:25741868), two supporting-level pathogenic criteria (PM2_Supporting, PP3_Supporting) are insufficient to reach Likely Pathogenic classification. The variant is classified as a Variant of Uncertain Significance (VUS).⁵