In AIP there is an abnormality in the haem biosynthetic pathway due to the deficiency of uroporphobilinogen I synthetase (porphobilinogen deaminase), which leads to excessive production of porphyrin precursors.1 The clinical features of AIP declare themselves at any stage from puberty onwards but mostly in the third decade of life. The gene discussed is HMBS; the disease is autoimmune pancreatitis.