Firstly, compound 73 obviously decreased the elevated levels of creatinine and urea and improved renal fibrosis and cellular damage in IRI rats by inhibiting oxidative stress via NF-κB/Nrf2 pathways, indicating that compound 73 could block AKI-to-CKD transition through regulating growth arrest-specific 6 (Gas6)/Axl-NF -κB/Nrf2 signaling cascade (Chen D. et al., 2019). This evidence concerns the gene GAS6 and chronic kidney disease.