The tumor immunity cycle is a process based on: a) a not-specific early phase driving the innate immunity that is mediated by macrophages, granulocytes, DCs and NK cells; b) late functional phase of effector CD4+ and CD8+ T-cells (Teffs) primed against melanoma cells through the endogenous production of interferon-gamma (IFN-γ), a direct cytotoxicity tumor resulting from MHC-TCR interaction or the antigen-dependent activity of T-cells during the adaptive immune response [38]. The gene discussed is HLA-C; the disease is neoplasm.