This hypothesis is further supported by our finding that mdx mice lacking both dystrophin and desmin (mdx‐Des−/−, dKO) presented an exacerbated cardiac phenotype, characterized by dilated cardiomyopathy according to standard criteria such as echocardiography data [50], elevated expression of cardiac stress markers (Nppa, Nppb, Myh7) [51, 52], and increased markers of myocardial fibrosis (Col1a1, Col3a1, Ctgf, Vim) [53]. This evidence concerns the gene DMD and dilated cardiomyopathy.