Multiple studies have demonstrated the prominence of apoptosis in the setting of AKI, and deletion of apoptosis‐associated proteins such as caspase‐8 or Fas from renal tubules has protected AKI.[26] Necroptosis is mediated by RIPK‐dependent phosphorylation of the MLKL and subsequent plasma membrane rupture, which is an important mediator of tubular injury. This evidence concerns the gene FAS and acute kidney injury.