Although the exact mechanism used by platelets to protect tumor cells from immunosurveillance is still debated, two hypotheses exist, namely: (a) release of platelet-derived factors like Interferon-gamma or transforming growth factor-beta1, inducing a reduced antitumor activity in NK cells; and (b) platelet-derived molecular mimicry of circulating tumor cells favored by an MHC class I molecules expression on the tumor cell membranes. Here, IFNG is linked to neoplasm.