For instance, sitagliptin can activate the p62–Keap1–Nrf2 signaling pathway to alleviate oxidative stress and excessive autophagy in acute lung injury, a mechanism that may also apply to OA improvement.[35] Furthermore, through a series of gain‐of‐function experiments, we demonstrated that DPP4 induces excessive mitochondrial fission, leading to oxidative stress and cellular senescence in chondrocytes, independent of its enzymatic activity. The gene discussed is DPP4; the disease is injury.