Many reports have provided evidence that CaMKII overactivity can induce potentially lethal ventricular arrhythmias by initiating DADs and causing pro-arrhythmic tissue remodeling that favors reentry (Aistrup et al., 2017; Curran et al., 2010; van Oort et al., 2010; Yoo et al., 2018). The gene discussed is CAMK2G; the disease is Ventricular arrhythmia.