Retention of mutated DMPK transcripts alters the levels and localization of important splicing regulators such as Muscleblind-Like Protein 1 (MBNL1) and CUGBP Elav-Like Family Member 1 (CELF) proteins, inducing splicing defect of several genes including Chloride Voltage-Gated Channel 1 (CLCN1), Insulin Receptor (INSR) or Bridging Integrator 1 (BIN1) responsible for cardiac conduction defect, diabetes and muscle weakness, respectively (Figure 2c) [60,61,62,63]. This evidence concerns the gene BIN1 and diabetes mellitus.