Cardiac‐specific activation of SGK1 in mice increased mortality rate as well as the incidence of cardiac dysfunction and ventricular arrhythmias, whereas SGK1 inhibition protected mice from fibrosis, heart failure, and sodium channel alterations.[18] Although there are commercially available SGK1 inhibitors, i.e., EMD638683 and GSK650394, the discovery of safer and highly specific SGK1 inhibitors with improved pharmacological properties gains great interest in the development of drugs for treating cardiac dysfunction and other associated diseases. This evidence concerns the gene SGK1 and Ventricular arrhythmia.