However, although harmine increased the levels of MBNL1 in DM1 myoblasts and enhanced MBNL1-dependent alternative splicing of cTNT E5, INSR E11, and Clcn1 E7a (Table S1 in Supplementary Material), a similar effect was found in wild-type myoblasts, suggesting that inhibition of the CUG–MBNL1 complex is not the primary MoA of this alkaloid. The gene discussed is INSR; the disease is myotonic dystrophy type 1.