On the other hand, the direct or CD16-dependent antitumor effector functions of NK cells are restrained by the action of a wide array of MHC class I-specific and nonspecific inhibitory receptors that negatively regulate their interaction with tumor cells and/or other components of the tumor microenvironment (TME) [6,8,31,32,33,34,35,36]. This evidence concerns the gene FCGR3A and neoplasm.