KCNH2, initially described and termed hERG, regulates IKr (rapid delayed rectifier K+ channel) and the blocking of IKr still remains a major issue in the development of antiarrhythmic drugs (Chen et al., 2000; Mitcheson et al., 2000; Mehta et al., 2018) in connection with the pharmacotherapy of LQTS at genetic levels (Mehta et al., 2018; Yin et al., 2018; Cortez et al., 2019; Kerr et al., 2019). This evidence concerns the gene KCNH2 and familial long QT syndrome.