Notably, while acute arsenic effects (2 μM-40 μM) are beneficial in managing NSCLC in experimental models, exposure to chronic low dose (100 nM or 0.5 μM) arsenic to normal human bronchial epithelial BEAS-2B cells has been shown to enhance cell proliferation and migration via mechanisms dependent upon the growth/ transcription factors or signaling pathways such as TGFα, EGFR, NRF2, and SOX9. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.