Consistently, the inducible Otub1 ablation greatly enhances antitumor immunity, characterized by increased numbers of tumor-infiltrating T cells, NK cells, and cDC1, and the intratumoral cDC1 increase in Otub1-deficient mice is dependent on NK cells.136 Otub1 regulates NK cell function by inhibiting IL-15-stimulated AKT ubiquitination and activation. Here, OTUB1 is linked to neoplasm.