The key mechanism that we elucidate here to account for upregulated CEMIP in human colon cancer dissemination is that hypoxia stabilizes HIF-2α, which can then bind to the CEMIP promoter, and inhibit the demethylase activity of Jarid1A, which leads to increased presence of H3K4me3 within the CEMIP promoter, ultimately resulting in increased CEMIP expression. The gene discussed is EPAS1; the disease is colonic neoplasm.