Mice engineered to model DM1-associated MBNL loss of function by a combined Mbnl1 and Mbnl2 knockout (31) or CELF1 gain of function by transgenic overexpression of human CELF1 protein (32) recapitulated several cardiac molecular and physiological disease features. This evidence concerns the gene MBNL2 and myotonic dystrophy type 1.