Moreover, protein expression levels of PARKIN, PINK1, p62, and LC3‐II/I in T2DM mice was 28.5%, 53.1%, 147.1%, and 55.9%, respectively, of that in healthy mice, and returned to normal levels after SENDs treatment, indicating that SENDs effectively ameliorated mitophagy defects under excessive oxidative stress by the PINK/PARKIN pathway (Figure 6F,G). The gene discussed is PINK1; the disease is type 2 diabetes mellitus.