Further research underlying anti-MM activity of IMiDs revealed two different mechanisms, a ubiquitin-dependent pathway with many factors playing a pivotal role such as ikaros (IKZF1) and aiolos (IKZF3), interferon regulatory factor 4 (IRF4) and interleukin-2 (IL2) [7], as well as an ubiquitin-independent pathway in which IMiDs bind to CD147-MCT1 complex instead of CRBN, producing an obstacle in tumor growth [8]. The gene discussed is IRF4; the disease is Miyoshi myopathy.