NK cells and CTLs, in a FasL, perforin, and granzyme B-dependent manner, induce apoptosis of melanoma cells [29, 30], while, in an IFN-γ and IL-17-dependent manner, enhance antigen-presenting properties of DCs and proinflammatory properties of tumor-infiltrating neutrophils, contributing to the generation of the strong antitumor immune response [31, 32]. The gene discussed is FASLG; the disease is neoplasm.