Unsurprisingly, in muscular dystrophy diseases, including sarcopenia, muscular dystrophy, and cancer-related cachexia, controlling myostatin signaling has become an attractive prospect for increasing functional muscle mass (Camporez et al. 2016; Smith and Lin 2013; Wei et al. 2016; Gallot et al. 2014; Weng et al. 2020). This evidence concerns the gene MSTN and muscular dystrophy.