This tumor cell killing effect is performed in different ways: (i) the activation of antiproliferative, proapoptotic, and angiostatic processes by IFN-γ, (ii) the production of reactive oxygen species (ROS) and reactive nitrogen intermediates by macrophages, and (iii) via TRAIL (TNF (Tumor necrosis factor) Related Apoptosis Inducing Ligand) or perforin-dependent mechanisms by NK cells [14]. The gene discussed is IFNG; the disease is neoplasm.