It is, therefore, reasonable to suggest that the functional B6 deficiency in AIP is based on modulation of Trp metabolism along the KP in a dual manner: an initial TDO activation by haem causing PLP depletion via enhanced KAT and Kynase activities, followed by HO 1 induction by haem, depriving TDO of its haem cofactor, thereby blocking production of Kyn metabolites that is essential for the PLP depletion. The gene discussed is TDO2; the disease is autoimmune pancreatitis.