TGFB1 and neoplasm: In addition to TGFβ, which can drive the conversion of circulating cytotoxic NK cells to poorly cytotoxic ILC1-like cells with impaired anti-tumor function and tissue-resident surface marker expression [103,121], exposing circulating NK cells to conditioned medium from decidual stromal cells or a combination of TGFβ, hypoxia, IDO, and demethylating agents, has also been shown to promote the acquisition of uNK phenotypic and functional attributes by peripheral blood NK cells [104,122,123,124].