Enhanced activity of immune effector cells in CMS2 immune-cold tumors (and indeed immune-hot CMS1 tumors) would not only enhance TNFα levels, but also levels of immune effector cell-associated death ligands FasL/CD95L and TRAIL in the tumor microenvironment, the anti-tumor activity of which is also enhanced by IAP antagonists58–61. This evidence concerns the gene TNF and neoplasm.