The interactions between MM cells and non-malignant cells from the bone marrow microenvironment—such as stromal and endothelial cells—contribute to elevated levels of interleukin 6 (Il-6), vascular endothelial growth factor (VEGF) and insulin-like growth factor 1 (IGF-1), which promote the PI3K/Akt/mTOR pathway’s activation [17]. Here, MTOR is linked to Miyoshi myopathy.