In classic EPP, there is a marked increase in free protoporphyrin, whereas in X-linked EPP there is also an increase in zinc chelated protoporphyrin; this is because the ferrochelatase enzyme is of normal activity and able to chelate some of the excess protoporphyrin with divalent metals such as zinc. The gene discussed is FECH; the disease is autosomal erythropoietic protoporphyria.