Concerning aorta‐derived MABs (Ao‐MABs) which have plasticity toward mesodermal derivatives, their injection intramyocardially leads to engraftment into the myocardium of dystrophic mice, and differentiation into CMs and ECs, thus preventing the onset of dilated cardiomyopathy.17 Similarly, it promoted angiogenesis and endogenous cardiac stem/progenitor cell proliferation in mdx/utrn−/− but not aged mdx mouse models for Duchenne muscular dystrophy. This evidence concerns the gene UTRN and dilated cardiomyopathy.