Consistently, recent studies have observed suppression of cell cycle withdrawal in DM1 or Celf1-overexpressing myoblasts (Furling et al., 2001; Peng et al., 2015), probably due to dysregulation of cyclin D1 and p21. DMPK, a rho kinase, may be involved in the regulation of myosin light chain phosphorylation, and its isoform E has been shown to be crucial for normal muscle development (Jansen et al., 1996; Mulders et al., 2011). This evidence concerns the gene DMPK and myotonic dystrophy type 1.