Early studies showed that under the influence of TGF-β, released by regulatory immune cells and myeloma cells, T cells presented a remarkable reduction in IL-2-mediated autocrine proliferation [167], and diverse signaling impairment, including the downregulation of CD28, CD152, p56lck, ZAP-70, and PI3K, which were found in both CD4+ and CD8+ T cells in MM patients with advanced-stage [173]. This evidence concerns the gene CTLA4 and Miyoshi myopathy.