In general, the prevalence of proinflammatory cytokine secretion [IL-1, IL-6, IL-12, IL-15, IL-16, IL-17, IL-18, IL-22, IL-23, tumor necrosis factor (TNF)-α and interferon (IFN)-γ)] versus anti-inflammatory secretion [heat shock proteins (HSPs), IL-1 receptor (IL1R)α, IL-4, IL-10, IL-11, transforming growth factor (TGF)-β1, and lipoxin A4)] in MM patients is contingent on genetic alterations that originate from the cells within the microenvironment [8]. This evidence concerns the gene IFNG and Miyoshi myopathy.