These molecules, i.e., myokine IL-6, pro-fibrotic TGF-β1, c-AMP dependent pathways and estrogen receptors, and all self-renewal mediators (e.g., G-CSF, Wnt7a, β1-integrin, p38MAPK, ghrelin derivatives), represent potential therapeutic targets of new/repurposed drugs for DMD to specifically support regeneration efficiency, via a direct action on satellite cells or by improving niche environment. Here, TGFB1 is linked to Duchenne muscular dystrophy.