More importantly, treatment of CC4 F(ab)2 remarkably blocked the repression of NK killing activity caused by either CEACAM1 or CEACAM5 ectopic expression, suggesting that the effect of mAb CC4 in enhancing the immune reaction against tumor cells is attributed to its function of specifically abrogating the initiation of CEACAM1 signaling in NK cells. This evidence concerns the gene CEACAM1 and neoplasm.