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. Here, MLKL is linked to acute kidney injury.