Previous studies demonstrated that DOX treatment caused myocardial damage and reduced phosphorylation of Akt and ERK1/2 [28], whereas activation of Ras/MEK/ERK and Akt signaling can inhibit DOX-induced apoptosis and ameliorate DOX-induced congestive heart failure [13], [18], [20], [28]. This evidence concerns the gene MAPK3 and congestive heart failure.