APEX1 and neoplasm: In our model, down‐regulation of circCIMT and APEX1, inhibited cell survival in the early stages of chronic Cd exposure, which relates to increased pressure on the cell replication machinery caused by aggravated DNA damage.[37, 38, 39] The increased proliferative ability of cells in the later stages of chronic Cd exposure may be attributed to abnormal amplification caused by instability of the cell genome.[40, 41, 42] More importantly, stable down‐regulation of circCIMT and APEX1 decreased the time taken for lung epithelial cells to acquire tumor characteristics following Cd exposure.