These molecular pathways include the hypoxia inducible factor-1 alpha (HIF-1α)-dependent induction and recruitment of Foxp3+ regulatory T cells (Tregs) through mechanisms involving TGF-β-driven STAT-3 signaling (15, 16), the release of CCL28 chemokine by tumor cells (17) and CCL22 by tumor-associated macrophages (TAMs) (18). The gene discussed is HIF1A; the disease is neoplasm.