Here, we demonstrate that ChA i) blocks monocyte chemotaxis, ii) kills M2, iii) activates nuclear factor kappa (NFκ)B and stress-activated protein kinases (SAPK)/c-Jun N-terminal kinase (JNK) in M1, but not in M2, connected with TNFα secretion, and iv) increases M1-mediated cytotoxicity for cancer cells in a TNFα-dependent fashion. This evidence concerns the gene TNF and cancer.