These findings are also consistent with emerging data demonstrating that conditional deletion of TIM-3 in DCs increases NLRP3 inflammasome activation in DCs, resulting in accumulation of IL-1β/IL-18 [16], therefore strengthening a function for TIM-3 in myeloid cells and supporting its broader role in the tumor microenvironment beyond that of checkpoint receptors in T cells. The gene discussed is NLRP3; the disease is neoplasm.