Both clinical histomorphometric analyses of bone samples from MM patients[31,32] and in vitro coculture studies using human MM cell lines [33] indicated that MMC inhibited OSB differentiation via downregulation of osteocalcin and collagen I. It has also been reported that in human osteoprogenitor cells, blocking of Runx2/Cbfa1 activity resulted in decreased OSB proliferation and activity,[32,34] suggesting multiple pathways could have also played a role in the observed declined in ALP activity in our coculture experiments. This evidence concerns the gene RUNX2 and Miyoshi myopathy.