In our study, the upregulation of MBNL1 by calcitriol seems to be beneficial in the DM1 model, since the abnormal splicing of MBNL1-regulated genes (Clcn1, Serca1, and Nfix) was partially corrected, and the muscle pathology as well as the muscle weakness was ameliorated. The gene discussed is MBNL1; the disease is myotonic dystrophy type 1.