To grasp the possible clinical relevance of the above findings, we have resorted to the CF disease because the IDO1/AhR axis has already been shown to be dysregulated24,25, the down-regulation of the CFTR abolishes the hypoxia-induced 5-HT release45 and 5-HT is among the top significant metabolites discriminating the metabolic profiles among CF mutations and lung function46. The gene discussed is AHR; the disease is cystic fibrosis.