These include whether decreased CBS activity contributes to the proinflammatory environment of AIP, do changes in KA and QA and their ratio play a role in the neurological features of acute attacks?, does an increase in KA promote PARP 1 expression by AhR activation to induce NAD+ depletion?, is there a potential occurrence of CBS and/or CγL variants in AIP?, does the functional B6 deficiency in AIP, particularly after givosiran or hemin therapy, modulate the Trp-metabolic activity in the GIT or resident microbiota to undermine their protective effects? This evidence concerns the gene CBS and autoimmune pancreatitis.