Antitumor effects of NK cells can be overcome by various approaches, for examples, conservation of MHC class I (MHC-I) expression, shedding of ligands for the activating NK receptor (e.g., NKG2DLs), and secretion of immunomodulatory molecules (e.g., TGF-β, prostaglandin E2, and adenosine) by tumor cells, ultimately resulting in tumor progression [50]. Here, TGFB1 is linked to neoplasm.