In cases of murine prostate cancer, mouse iNKT cells directly targeted M2-like macrophages through CD1d recognition and engagement of Fas-FasL mediated killing to reduce tumor burden; in addition, CD40L presentation to APCs motivated crosstalk with other effector cells to dampen the pro-angiogenic and immunosuppressive capabilities of tumor-infiltrating immune cells, delaying prostate tumor growth (53). This evidence concerns the gene FASLG and neoplasm.