“…Myonecrosis, sarcolemmal disorganization, inflammation, and the accumulation of fibro-fatty scar tissue are observed early in DMD and increase with age (Cáceres et al, 2000;Porter et al, 2002;Reed and Bloch, 2005;Serrano et al, 2011;Grounds et al, 2020). Remarkably, FAPs generate activated fibroblasts, myofibroblasts, adipocytes, and bone-like cell progeny in muscular dystrophy, albeit to different extents depending on the degree of damage, inflammation and degeneration (Uezumi et al, 2011(Uezumi et al, , 2014Lemos et al, 2015;Contreras et al, 2016Contreras et al, , 2019aIeronimakis et al, 2016;Kopinke et al, 2017;Eisner et al, 2020;Mázala et al, 2020). As known for other muscle-resident cells, the exit of FAPs from quiescence and their entry into proliferative and differentiation programs are not only finely tuned by microenvironmental cues (Uezumi et al, 2010;Heredia et al, 2013;Moratal et al, 2018Moratal et al, , 2019 but also through intrinsic molecular mechanisms like epigenetic HDAC-dependent pathways (Mozzetta et al, 2013;Saccone et al, 2014;Sandonà et al, 2020) or Hic1-dependent quiescence maintenance (Scott et al, 2019;Contreras, 2020).…”