As anticipated, the disordered ferroptosis markers in the AKI mouse model, including increased 4-hydroxynonenal (4-HNE), damaged mitochondrial morphology, and dysregulated expression levels of GPX4, were also ameliorated in RestRTKO mice, with a further amelioration in Fer-1–treated mice (Figure 7, A–C). The gene discussed is GPX4; the disease is acute kidney injury.