c.38G>T (p.Gly13Val) is located in the P-loop domain (residues 10-17), an approved functional domain critical for GTP binding and hydrolysis in NRAS, satisfying PM1 at moderate strength per the ClinGen RASopathy VCEP.¹ PP2 is met at supporting strength as this is a missense variant in NRAS, a RASopathy gene where missense variants are a common mechanism of disease, per the VCEP specification.² Multiple in silico tools predict a deleterious effect (REVEL = 0.789, BayesDel = 0.314), satisfying PP3 at supporting strength per the VCEP.³ The variant is present at extremely low frequency in gnomAD (v2.1: 1/251,492; v4.1: 1/1,614,026) and is absent from gnomAD-Canada, consistent with a rare disease-causing variant, though PM2 is not met per strict VCEP requirement for complete absence.⁴ The variant has been reported in ClinVar as Likely pathogenic by two clinical laboratories (ClinVar ID 375876) and is annotated as Likely Oncogenic by OncoKB with 141 somatic occurrences in COSMIC, supporting its functional significance, though these alone do not independently meet PS4 or PS5 criteria per VCEP rules.⁵ PVS1, PP5, BP6, PP4 are not applicable per the RASopathy VCEP specification. BP1 is not applicable as this is a missense variant, not a truncating variant. BP7 is not applicable as this is not a synonymous variant.⁶