In various cancers like glioblastoma, lung, breast, etc., M1 (classically activated or pro-inflammatory) macrophages are attracted by chemotaxis (towards cytokines released by CSCs) to the tumor site where they get converted to M2 (alternatively activated or anti-inflammatory or tumor-associated) macrophages, secreting TGF-β, IL-10, IL-23, and arginase 1 that creates immune-suppressive tumor microenvironment for tumor growth [149–152]. This evidence concerns the gene IL10 and neoplasm.