As a crucial regulator of genomic stability, mutations in the POLE gene have been implicated in accelerating tumor progression through potential impacts on the MMR pathway, TGF‐β signaling, and the RTK/RAS/RAF pathway.[48] In DEE‐OEs‐induced malignant transformation cells, MMR pathway abnormalities and activation of classic lung cancer‐related signaling pathways were indeed observed; these changes are closely associated with POLE deficiency‐induced genomic instability, forming a vicious cycle that further drives tumor development. This evidence concerns the gene TGFB1 and neoplasm.