Existing research has suggested that the response of TAMs in the complex TME is largely biased toward the alternative activation phenotype M2, where M2 macrophages up-regulate CD163, interleukin-10 (IL-10), mannose receptors, and arginase-1 (Arg-1) while facilitating tumor neoangiogenesis and suppressing anti-tumor immunity. This evidence concerns the gene CD163 and neoplasm.