Patients harboring pathogenic PTPN11 or SOS1 variants have a low prevalence of hypertrophic cardiomyopathy [3], while those with disease-causing RAF1, RIT1 and MRAS variants are expected to develop this cardiac defect (~85%, 70%, and 100%, respectively) [4,5,6], showing the strongest association with HCM among RASopathies [7]. This evidence concerns the gene RAF1 and hypertrophic cardiomyopathy.