Oral or intravenous carbohydrate surplus, leading to an increment in insulin levels, have been associated with low biochemical disease activity in a case-control study including 50 patients with AIP, probably due to phosphatidylinositol 3-kinase (PI3K)/Akt-mediated ALAS1 inhibition [72,75]. Here, ALAS1 is linked to autoimmune pancreatitis.