We have focused on the negative feedback provided by CYP1A1 to control AHR activation via ligand metabolism and shown that Cyp1a1 overexpression and excessive metabolic activity results in more severe psoriasis-like skin inflammation in mice [104], a direct phenocopy of the exacerbated pathology observed in mice lacking Ahr [92], possibly due to reduced ligand availability, as shown in the gut [20]. The gene discussed is AHR; the disease is dermatitis.