Salih and colleagues explored various mechanisms, including the down-regulation of NKG2D on NK cells by platelet-derived TGF-β, platelet-derived MHC class I transfer onto the tumor cell surface, and forward signals from platelet-expressed glucocorticoid-induced TNF-related ligand (GITRL) to GITR on NK cells that result in the impaired anti-tumor reactivity of NK cells (109–111). The gene discussed is TGFB1; the disease is neoplasm.