More significantly, our finding revealed that DPP-4i also triggered NF-кB-dependent NLRP3 inflammasome activation, leading to caspase-1-mediated processing of IL-1β and IL-33, two critical proinflammatory cytokines for the tumor-immune-suppressive microenvironment (21, 22). The gene discussed is NLRP3; the disease is neoplasm.