Under pathological conditions, the crosstalk between JAK/STAT3 and hypoxia/HIF1α pathways is significant: rheumatoid arthritis is an autoimmune disease characterized by high levels of inflammation due to the crosstalk between STAT3 and hypoxia pathways [18]; glucose deprivation in brain pericytes is regulated by STAT3-mediated induction of HIF1α [19]; the self-renewal of glioma stem-like cells, which was previously considered as a hypoxia-dependent mechanism, appeared to be determined by an upregulation of STAT3 by HIF1α [20]. Here, HIF1A is linked to rheumatoid arthritis.