Notably, the Lior Gepstein lab reported that iPSC-CMs, derived from dermal fibroblasts from a symptomatic SQTS patient having an N588K variant in the KCNH2 gene exhibited: 1) shortened APD, 2) increased IKr current density, and 3) increased channel protein expression compared to the healthy and isogenic controls at the cellular level (Shinnawi et al., 2019). This evidence concerns the gene KCNH2 and Familial short QT syndrome.