In the tumor microenvironment, autophagy is triggered by binding of IL-6 and CCL2 to interleukin 6 receptor (IL-6R) and CCR2, respectively, which is essential for macrophage polarizaton to the M2 phenotype, resulting in increased anti-inflammatory cytokine secretion, which promotes the fading of inflammation as well as tissue repair and remodeling, but M2 macrophages are immunosuppressive cells [101, 104–106]. The gene discussed is IL6R; the disease is neoplasm.