Additionally, research by Fenget al. (2021) [61] on the KCNH2 mutation hERG1-p.H70R iniPSC-CMs models suggests these mutations lead to decreased IKrcurrents and accelerated deactivation in cardiomyocytes, directly contributing toprolonged APD and consistent with the LQTS phenotype. This evidence concerns the gene KCNH2 and familial long QT syndrome.