Moreover, hypoxia arises as a consequence of low oxygen levels in the tumor microenvironment, leading to the activation of hypoxia-inducible factor-1α (HIF-1α), which activates genes to promote CSC survival, proliferation, angiogenesis, and drug resistance, including octamer-binding transcription factor 4 (OCT4), nanog homeobox (NANOG), SRY-box transcription factor 2 (SOX2), vascular endothelial growth factor A (VEGFA), and ATP-binding cassette sub-family G member 2 (ABCG2) [27,28]. The gene discussed is ABCG2; the disease is neoplasm.