Notably, dysregulation of 14‐3‐3 target proteins has been implicated in various human diseases, including DM and cancer.[23] In our study, overexpression of 14‐3‐3ε in RPE cells effectively rescued PDZK1‐mediated suppression of mTOR signaling and cell senescence, suggesting that the PDZK1‐14‐3‐3ε‐mTOR axis plays a critical role in high‐glucose‐induced RPE cell senescence. The gene discussed is PDZK1; the disease is diabetes mellitus.