Indeed, within HCC tumor lesions, MAIT cell frequency was reduced compared to peritumoral hepatic area and the HCC microenvironment polarized tumor-infiltrating MAIT cells to an exhausted phenotype (PD-1high CTLA-4+ TIM-3+), leading to a reduced response to bacterial antigens and the production of tumor-promoting cytokines (69). The gene discussed is HAVCR2; the disease is neoplasm.