Wu’s group revealed DTNs (≈18.79 nm) possessed therapeutic potential against ferroptosis in cis-AKI, where it could rescue renal proximal tubular epithelial (HK-2) cells treated with ferroptosis-inducer in vitro through reducing lipid ROS as well as reversing the downregulation of glutathione peroxidase 4 (GPX4) in both transcription and translation level [108] (Figure 5a). The gene discussed is GPX4; the disease is acute kidney injury.