We can draw several conclusions from the present study, as follows: 1) aberrant CaMKIIδB expression is associated with a disturbance in SR Ca2+ content and an imbalance of NCX1/SERCA2 in TAC-induced heart failure; 2) active CaMKIIδB up-regulates NCX1 protein expression in adult cardiomyocytes via HDAC/MEF2-dependent signaling; and 3) the antagonism of calmodulin restores SR Ca2+ levels and regulates the imbalance between NCX1 and SERCA2 by inhibiting CaMKIIδB activity, then rescues cardiomyocytes from apoptosis and improves cardiac function. The gene discussed is ATP2A2; the disease is heart failure.