Retained cytosolic calcium due to the Δ160E mutation could activate calcineurin, a serine/threonine-specific phosphatase that plays a crucial role in the development of cardiac hypertrophy.31 Calcineurin dephosphorylates NFATc1 and promotes translocation from the cytosol into the nucleus, which accelerates pro-hypertrophic gene expression.32 Therefore, nuclear signals raised from NFATc1 in Homo-Δ160E-iPSC-CMs represents the direct downstream change caused by retained calcium and can be the useful readout for therapeutic screening. Here, NFATC1 is linked to cardiac hypertrophy.