Moreover, Ripk3−/− to Ripk3−/− chimeric mice displayed better protective effect in the long term after IRI than Ripk3+/+ to Ripk3−/− by more strongly inhibiting inflammasome activation and IL-1β release, suggesting that deletion of Ripk3 or Mlkl in immune cells contributed to alleviating AKI to CKD by preventing NLRP3 inflammasome activation. The gene discussed is RIPK3; the disease is acute kidney injury.