Overexpression of hnRNP A1 in differentiated myoblasts leads to muscle pathology by antagonizing the activity of MBNL1 and inducing DM1-associated fetal-specific alternative splicing patterns, suggesting that it may function to promote myoblast proliferation and inhibit myogenic differentiation (Li et al., 2020). This evidence concerns the gene MBNL1 and myotonic dystrophy type 1.