Thus, we propose that the inhibitory effect of the calmodulin antagonist on CaMKIIδB activity contributes to rescue from CaMKII-mediated up-regulation of NCX1 during TAC-induced hypertrophy, which maintains the balance of NCX1/SERCA2 and strengthens the SR Ca2+ concentration. The gene discussed is ATP2A2; the disease is persistent truncus arteriosus.