Proinflammatory TLR9/AHR responsiveness has been linked to worsened IPF progression (30); however, the functional binding partners of AHR in inflammatory versus normal conditions, the triggers that divert AHR from its canonical pathway, and the exact role of AHR in complex pathologies such as fibrosis are not well understood. This evidence concerns the gene AHR and idiopathic pulmonary fibrosis.