Recently, we showed that in mice subjected to pressure overload, chronic CaMKII inhibition: (a) preserved conduction velocity, expression and localization of the gap junction protein Cx43 and Nav1.5 sodium channels, (b) did not prevent hypertrophy and fibrosis formation and consequently and (c) did not prevent heart failure and arrhythmogenesis7). This evidence concerns the gene CAMK2G and heart failure.