Genomic instability is a hallmark of cancer, typically associated with mutation accumulation, chromosomal rearrangements, and defects in DNA repair mechanisms, which collectively increase the likelihood of oncogene activation and tumor suppressor gene inactivation, ultimately promoting tumorigenesis.[50] In the DEE‐OEs‐induced malignant transformation cells, we observed downregulation of tumor suppressor genes such as PTEN, CASP8, and CDKN1A, along with significant activation of oncogenes including EGFR, JAK, and STAT3. The gene discussed is STAT3; the disease is cancer.