The activation of NLRP3 inflammasome has been proved to contribute to the inflammatory response of sepsis-induced AKI, which causes an impaired kidney morphology, increased renal tubular cell apoptosis, and NLRP3-dependent proinflammatory cytokine (i.e., IL-1β and IL-18) production [8–10]. Here, NLRP3 is linked to Sepsis.