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. This evidence concerns the gene MLKL and acute kidney injury.