MBNL1 and myotonic dystrophy type 1: In vitro and in vivo efforts to develop DM1 therapeutic strategies have been mostly aimed at destroying the toxic ribonucleoprotein complexes via targeting the mutant CUGexpRNA and/or inhibiting its pathogenic interactions with MBNL1 protein, leading to the generation of several strategies that proved to have a beneficial effect in DM models (17, 18).