The primary gene (SCN5A) encodes the pore-forming alpha subunit of the primary Na+ channel (Nav1.5) in the human heart (Lieve et al., 2017; Verkerk et al., 2018), and this so-called “gain-of-function mutation” determines the late Na+ current (INa), which leads to (i) the development of one type of long-QT syndrome (LQTS), (ii) the prolongation of the duration of the AP, and (iii) the genesis of premature ventricular contractions in myocardial cells (Keating and Sanguinetti, 2001; Splawski et al., 2002; Wang et al., 2004; Amin et al., 2018). Here, SCN5A is linked to familial long QT syndrome.