Similarly, Cong et al. revealed that NK cells in the TME are influenced by transforming growth factor-β (TGF-β), prostaglandin E2 (PGE2) and interleukin (IL)-10 secreted by tumor cells; moreover, the up-regulation of fructose-1,6-bisphosphatase (FBP1), a key enzyme of gluconeogenesis, inhibits the glycolysis of NK cells, reducing their anti-tumor activity [29]. The gene discussed is TGFB1; the disease is neoplasm.