In this disease, the mutant mRNAs (which contain expanded CUG trinucleotide repeats, and are called CUG-RNAs) are thought to interact with, and deregulate, splicing modulators, such as the muscleblind-like protein 1 (MBNL1), driving the main pathogenic effect in DM1. This evidence concerns the gene MBNL2 and myotonic dystrophy type 1.