After ILC1s have arisen in the periphery, it is plausible that they acquire a spectrum of organ- and cancer-specific effector phenotypes through a unified Hobit-dependent differentiation pathway that is fine-shaped by local factors, e.g., TGFβ or, as shown by the authors, cancer-derived IL15.4 Besides the IL-2/IL-15R β chain also other surface molecules, such as TRAIL, NKG2D, and NKp46 are involved in the sensing and elimination of malignant cells. Here, IL15 is linked to cancer.