Of note, splicing changes may underlie this effect, because WT mice expressed mainly the α2 splice isoforms of Mef2c and Mef2d, which act cooperatively with Myog and Myod1 to promote myogenic differentiation and sustain muscle gene expression (41,42), whereas DM1 models expressed higher levels of the α1 isoforms (Supplemental Figure S3), which antagonize α2 isoforms and interact with inhibitory class II histone deacetylases that repress gene expression (43–47). The gene discussed is MYOD1; the disease is myotonic dystrophy type 1.