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. This evidence concerns the gene ATP2A2 and persistent truncus arteriosus.