Importantly, while we have provided validation of the effectiveness of SGK1 inhibition by small-molecule compounds to shorten the pathological APD in LQT3 iPSC-CM models and have shown for the first time the efficacy of SGK1-I to shorten the APD in patient-specific iPSC-CM models of LQT1 and LQT2, further studies in additional human iPSC-CM models of LQT1, LQT2, and LQT3 with unique pathogenic variants with differing underlying cellular mechanisms of disease are warranted. Here, SCN5A is linked to long QT syndrome 3.