EZH2 and Miyoshi myopathy: Overexpression of LSD1 in BMSCs blocked Wnt signaling pathway by demethylating H3K4 and epigenetically silencing pro‐osteogenic Wnt‐gene promoters (Fig. 2).91 In addition, knockdown of LSD1 or its partner REST corepressor 2 (rcor2) blocked adipogenesis and increased expression of inflammatory cytokines and chemokines in 3T3‐L1 preadipocytes.93 Collectively, these results suggest that the use of small molecule inhibitors to epigenetically target EZH2, HDAC1, and LSD1 could reverse adipogenic differentiation that occurs at the expense of suppressed osteogenesis and promote bone repair in MM.