FXR activation by GW4064 has been shown to attenuate cisplatin‐induced AKI by suppressing ferroptosis through the transcriptional regulation of ferroptosis‐related and antioxidant genes [34], In our prior study, we found that FXR activation upregulated fatty acid oxidation (FAO)‐related genes, improved FAO in proximal tubular epithelial cells, causing a reduction in lipid accumulation and mitigation of kidney damage [16]. This evidence concerns the gene NR1H4 and acute kidney injury.