Since cell proliferation in MM is closely linked to increased energy expenditure associated with glucose metabolism, and the greater the malignancy of the tumor, the higher the energy demands, it is therefore possible that the stronger expression of Metrnβ in MM may represent a compensatory anti-tumor response by the host based on the pleiotropic effects of Metrnβ in improving insulin sensitivity, maintaining glucose homeostasis, promoting white fat browning, and increasing energy expenditure [9]. This evidence concerns the gene INS and Miyoshi myopathy.