SOAT1 and Miyoshi myopathy: Furthermore, along with disease evolution, an increase in the activation of the JAK/STAT signaling in response to MM cells exposure has been observed, which, coupled with MDSCs’ capability to differentiate into “osteoclast-like” cells to deplete arginine from the microenvironment through overexpression of arginase-1 and to increase nitric oxide production, supports the establishment of a proinflammatory and tolerogenic niche as well as the generation of lytic bone lesions [15,24,25,28].