The concept that combined deficiency in pro-inflammatory and necroptotic signaling in these models switches the etiopathology at onset completely toward ferroptosis, which we have proved, although only in the AKI model with necroptotic-resistant Mlkl knockout mice (Müller et al., 2017), can be verified only after developing durable, less serum-labile ferroptosis inhibitors. The gene discussed is MLKL; the disease is acute kidney injury.