On the other hand, the subsequently produced cytokines (TNF-α, Fas ligand (FasL), TNF-related apoptosis-inducing ligand (TRAIL), etc.)can also be exploited to induce tumor cell killing beyond the zone of initial infection, facilitated via co-treatment with a number of different pharmaceutical agents, such as SMAC-mimetic compounds (SMCs) [154,171,172] and B cell lymphoma-2 (BCL-2) homology domain 3 (BH3) mimetics [173,174]. This evidence concerns the gene TNF and neoplasm.