This opposite result of HIF‐2α regulation of inflammation and cancer in the intestine is due to the fact that in the colon tumor microenvironment, HIF‐2α is able to directly regulate a potent neutrophil chemokine, CXCL1, resulting in overexpression of HIF‐2α promoting the recruitment of neutrophils to colon tumors and promoting tumor proliferation [28]. This evidence concerns the gene EPAS1 and colonic neoplasm.