TGFB1 and neoplasm: In this context it needs to be emphasized that ILC1s also have the potential to promote tumor growth depending on the tissue context and ILC1 phenotype, e.g. as it was shown for fibrosarcoma progression in a murine cancer model.1,3 Here, a mechanism of tumor immunoevasion was demonstrated in which TGFβ-driven conversion of NK cells into ILC1s leads to a suppressed antitumor immune response and thus enhanced tumorigenesis.4 Future studies are needed to unravel the heterogeneous functional programs and plasticity of tissue-resident ILC1s within different types of cancer.