The pro-inflammatory/anti-tumorigenic M1 phenotype is induced by factors such as tumor necrosis factor-α, interferon (IFN)-γ, and lipopolysaccharide (LPS), and is characterized by the expression of CD86 and inducible nitric oxide synthase (iNOS), and the anti-inflammatory/tumor-promoting M2-like phenotype is triggered by interleukin (IL)-4 and IL-13, stimulating the and expression of CD163, CD206, and arginase-1 (Arg-1) [7]. The gene discussed is CD163; the disease is neoplasm.