These findings are consistent with previous observations that CnA expression and activity of calcineurin increases under physiological stressful conditions, including heart failure[39] and hypoxia[40], and that inhibition of CnA can attenuate myocardial infarction.[41] The current study has demonstrated that the addition of CnA siRNA inhibited the expression of dephosphorylated Drp1. Here, PPP3CA is linked to myocardial infarction.