CAMK2G and dilated cardiomyopathy: The coexpression of mtCaMKIIN reversed the dilated cardiomyopathy phenotype in the mtCaMKII mice (Fig. 2d), without reducing mtCaMKII expression (Fig. 2e, f), confirming that dilated cardiomyopathy is due to excessive mitochondrial CaMKII activity, and excluding the possibility that dilated cardiomyopathy is a non-specific consequence of mitochondrial-targeted transgenic protein overexpression.