Both in in vivo and in vitro model of DOX-induced cardiomyopathy and cardiomyocyte apoptosis, we demonstrated that SMI could alleviate DOX-induced cardiotoxicity, improve cardiac function, and maintain mitochondrial homeostasis through activation of AMPK and PI3K/Akt/GSK-3β signaling pathway (Figure 9). This evidence concerns the gene GSK3B and cardiomyopathy.