In order to increase the functional pool of MBNL in DM1 cells/tissues and alleviate pathogenesis of DM1 by the reversal of aberrant alternative splicing, the expression of MBNL1/2proteins has been increased by using nonsteroidal anti-inflammatory drugs such as phenylbutazone (PBZ) and ketoprofen [138], and antiautophagic drugs such as chloroquine [139], or by delivery of recombinant-adeno-associated-virus (rAAV) vectors carrying MBNL1 [120] (Table 2). The gene discussed is MBNL1; the disease is myotonic dystrophy type 1.