SKIL and neoplasm: In the tumor microenvironment characterized by high levels of TGF-β, NK1 and NK5 clusters exhibited low expression of TGFBR2 (with particularly low levels in the NK5 cluster) and simultaneously up-regulated negative regulators of TGF-β signaling, SKI, SKIL, and TGIF1, indicating that these NK clusters may be adapting to mitigate the suppressive effects of TGF-β.