Because of the reciprocal antagonism of IL-15 and TGFβ on intracellular signaling pathways [41], [42], [43], we wondered if decreased NKG2D expression on circulating NK cells from HCV patients might be amplified by a resistance of NK cells to endogenous IL-15 due to TGFβ or by a defective production of IL-15 in response to infection. Here, KLRK1 is linked to infection.