NM_033360.3:c.179G>T (p.Gly60Val) is a missense variant in KRAS identified in a single de novo proband with Noonan syndrome and lethal hypertrophic cardiomyopathy (Nosan et al. 2013).¹ The variant affects Gly60, which resides in the Switch II domain (AA 57–64), a critical functional domain per RASopathy VCEP specifications (PM1_Moderate).² At least two different pathogenic missense changes (p.Gly60Ser, p.Gly60Arg) have been reported at the same codon in RASopathy patients, satisfying PM5 at Moderate strength.³ Parental genotyping confirmed the variant occurred de novo, meeting PS2 at Moderate strength (1 de novo point per VCEP rules).⁴ The variant is observed in a single RASopathy proband, meeting PS4 at Supporting strength (≥1 point per VCEP rules).⁵ REVEL in silico score of 0.879 exceeds the VCEP threshold of ≥0.7, meeting PP3 at Supporting strength.⁶ The variant is present at extremely low frequency in gnomAD (v2.1: 1/251,328; v4.1: 3/1,614,068), which is below benign population thresholds but above the PM2 absence requirement.⁷ Applying the RASopathy VCEP classification rules: three Moderate criteria (PS2_Moderate, PM1, PM5) plus two Supporting criteria (PS4_Supporting, PP3) are met. Per VCEP Rule13, ≥3 Moderate criteria yields a classification of Likely Pathogenic.⁸