The success of immunotherapies, such as checkpoint blockade, has highlighted the importance of the immune system in controlling tumours. The presence of conventional T cells within the tumour microenvironment have been intensively studied and correlates with patient outcomes, however, the role of mucosal-associated invariant T (MAIT) cells in cancer is relatively unknown. MAIT cells are abundant in humans and enriched in mucosal tissues, such as the colon and lung, and some recent studies have reported the presence of these cells within primary and metastatic tumours. Our recent publication1 shows that MAIT cell-deficient mice have enhanced NK cell-dependent control of metastatic B16F10 tumour growth relative to control mice. Analyses of this interplay in human tumour samples revealed that high expression of a MAIT cell gene signature negatively impacts the prognostic significance of NK cells. Paradoxically, pre-pulsing tumours with MAIT cell antigens, or activating MAIT cells in vivo, enhances anti-tumour immunity in B16F10 and E0771 mouse tumour models, including in the context of established metastasis. These effects are associated with enhanced NK cell responses and increased expression of both IFNγ-dependent and inflammatory genes in NK cells. Importantly, activated human MAIT cells also promote the function of NK cells isolated from patient tumour samples. Our results thus describe an activation-dependent, MAIT cell-mediated regulation of NK cells, suggesting a potential therapeutic avenue for cancer treatment