TGFB1 and Miyoshi myopathy: In fact, BM-MSCs of MM patients internalize MM plasmocyte-derived EVs through endocytosis, micropinocytosis and membrane fusion (136), and these EVs are enriched in miR-146a and miR-21, which influence the altered BM-MSCs to secrete cytokines such as IL-6 and TGFβ to establish a ME favorable for MM growth and migration (137).