HIV-1 infection induces pro-IL-1β production in monocytes by activating TLR8 and subsequently activates caspase-1 through the NLRP3 inflammasome, leading to the cleavage of pro-IL-1β into its bioactive form, IL-1β, underscoring the essential roles of both TLR8 and NLRP3 in HIV-1-induced inflammation. The gene discussed is IL1B; the disease is HIV-1 infection.