Once formed, the NLRP3 inflammasome activates caspase-1, which subsequently mediates the cleavage of pro-IL-1β and pro-IL-18 and the secretion of their bioactive forms, important players in the systemic inflammation and cardiac dysfunction (and MOF) during sepsis (81–83, 99, 100). The gene discussed is NLRP3; the disease is Sepsis.