hiPSC-CMs derived from two independent patients carrying the heterozygous pathogenic variant p.Thr468Met in PTPN11 showed a significant increase in cell size and a higher proportion of cells with nuclear NFATC4 localization (80 % vs. 30 %), a key regulator of cardiac hypertrophy, compared to hiPSC-CMs derived from a healthy brother of one of the patients, recapitulating the HCM observed in patients with Noonan syndrome with multiple lentigines [28]. This evidence concerns the gene PTPN11 and Noonan syndrome.