Since mitochondrial calcium overload caused by increased activation and expression of RIPK1 is the core mechanism of DCM induced by TAB2 knockdown in cardiomyocytes, we hypothesized that the administration of the RIPK1 inhibitor Nec-1s to KO cardiomyocytes would ameliorate the DCM phenotype. Here, TAB2 is linked to familial dilated cardiomyopathy.