On the contrary, in a specific subset of MM (non-hyperdiploid type and with c-MAF or MAF-B translocation) and thyroid carcinoma, Deptor behaves like an oncogene, as its overexpression results in mTORC1 activity inhibition and a contemporary Akt activation, promoting cancer cells survival [2, 42, 43]. This evidence concerns the gene MAF and Miyoshi myopathy.