In the other, X-linked protoporphyria (XLP), ferrochelatase levels are normal, but there is a gain of function in the first pathway enzyme, ALAS2 which leads to the production of protoporphyrin that is in excess over what the levels of ferrochelatase normally present can metabolize (Whatley et al., 2008). This evidence concerns the gene ALAS2 and X-linked lymphoproliferative disease.