In summary, our current study has further confirmed the protective role of FGF1 on DN with attenuation of renal fibrosis and glomerulosclerosis, and demonstrated that FGF1 administration blocked diabetes‐induced oxidative stress level though NOX2‐ROS‐Nrf2 signalling, and elevated ER stress (Figure 6), suggesting that reduction of cellular stress is another potential mechanism underlying FGF1 treatment for DN. This evidence concerns the gene CYBB and renal fibrosis.