Our previous data indicate that HIF-1α upregulation during chronic, protracted inflammation—as in the case of Crohn’s disease—renders Th17 cells refractory to AhR-mediated immunoregulation, suggesting that CD39 regulation at the transcriptional level is subjected to a certain degree of modulation that might depend on inflammatory statuses as well as environmental triggers20. This evidence concerns the gene HIF1A and Crohn disease.