TAMs display an alternatively activated M2 phenotype known to be critical in controlling tissue homeostasis and wound healing; however, in the tumor, this phenotype is undesirable since it enables potent T cell inhibition via cytokines (e.g., IL-10), depletion of key metabolites (expression of arginase, IDO), or by contact inhibition (e.g., via PD-L1) [95]. This evidence concerns the gene IL10 and neoplasm.