In young mdx mice, a Duchenne muscular dystrophy model, HDAC inhibitors (HDACis) enhance MyoD and BAF60c expression, upregulate myogenic microRNAs (e.g., miR-1, miR-133, and miR-206), and suppress BAF60a/b, thereby promoting the myogenic conversion of FAPs while inhibiting adipogenic and fibrogenic fates (Saccone et al., 2014). This evidence concerns the gene SMARCD3 and Duchenne muscular dystrophy.