Several studies have shown that the limited availability of functional MBNL1, MBNL2, and/or MBNL3 contributes considerably to the development of molecular features of DM1 (Osborne et al., 2009; Du et al., 2010; Batra et al., 2014; Goodwin et al., 2015), as well as relevant phenotypes in mice (Kanadia et al., 2003; Matynia et al., 2010; Charizanis et al., 2012; Lee et al., 2013; Choi et al., 2015; Dixon et al., 2015; Thomas et al., 2017). This evidence concerns the gene MBNL1 and myotonic dystrophy type 1.