When type I NKT cells are stimulated by exogenous agonistic antigens such as α-GalCer, activated type I NKT cells exert their anti-tumor activity through two mechanisms: direct killing of CD1d-expressing tumor cells and facilitation of anti-tumor immune responses through induction of effectors cells, including NK cells and CD8+ T cells, via the production of cytokines such as IFN-γ (Figure 1). The gene discussed is IFNG; the disease is neoplasm.