As already described for SG g1 ILCs, the conversion of tumor-infiltrating NK cells towards intILC1s was also shown to be dependent on TGF-β-R2 signaling [21], [62], indicating that the tumor microenvironment (TME) can alter the phenotype of infiltrating NK cells through the release of TGF-β, further promoting the expression of inhibitory receptors and exhaustion markers, like NKG2A, CTLA-4, and LAG-3. This evidence concerns the gene TGFBR2 and neoplasm.