In the Dystrophin−/− (Dmd1)/Utrophin−/− (Utrn) cardiomyopathy model, Cldn5 mRNA and protein levels decline [129]; in contrast, Cldn5 overexpression diminishes cardiomyopathy in Dmd1−/−:Utrn−/− mice [128]. This evidence concerns the gene CLDN5 and cardiomyopathy.