In MM patients, the osteogenic ability of mesenchymal progenitors to differentiate to mature OBs is disrupted [57,58,59], as evidenced by the decrease in the levels of Osterix, the major osteoblast transcriptional activator, and of the bone formation markers, i.e., ALPL and Collagen type I α1 chain [60,61,62]. The gene discussed is ALPL; the disease is Miyoshi myopathy.