They exert their cytotoxic activity by distinct mechanisms, including the release of granzymes and perforin, secretion of IFN-γ and TNF-α, the expression of the FasL/Fas or TNF-related apoptosis-inducing ligand (TRAIL)/TRAIL receptors and the antibody-dependent cell-mediated cytotoxicity (ADCC) via Fc receptors (CD16) recognizing antibodies bound to antigen-coated (tumor) cells (4–6). The gene discussed is TNF; the disease is neoplasm.