MEIS2 and Miyoshi myopathy: Reduced expression of MEIS2 also increased the activity of different anti-MM chemotherapics able to affect molecular pathways critical for MM biology such as genotoxic and proteotoxic stress (e.g. Melphalan, Bortezomib), the function of molecular chaperones important for correct folding and function of client proteins (e.g. 17AAG/HSP90), the activity of epigenetic readers of acetylated histones (e.g. JQ1/BRD4), or to modify the function of molecular targets (e.g. Lenalidomide/CRBN) (Fig. 2).