The ensuing finding that APPL1 knockdown led to higher cell apoptosis rates and increased the protein levels of pro-apoptotic-proteins, Bax and cleaved PARP, and reduced anti-apoptosis protein Bcl-2 protein levels that participated in the apoptosis induced by myocardial ischemia/reperfusion [32,33]. This evidence concerns the gene APPL1 and myocardial ischemia.