GJA1 and ventricular tachycardia: Iravanian et al. [23] and Sovari et al. [24] reported that RAS inhibition in mice with cardiac-specific angiotensin converting enzyme overexpression, which exhibited proclivity to ventricular tachycardia (VT) and sudden death because of the reduced Cx43, could increase the total amount of Cx43 and its phosphorylated counterpart, decrease VT inducibility and increase the survival rate, indicating that intervening RAS could attenuate the impairments of Cx43.