The selective accumulation of PpIX in HGG, but not in normal tissue, is explained by a variety of different mechanisms: the limited activity of ferrochelatase, an enzyme for PpIX metabolism to heme, in tumor cells; the increased capacity for converting 5-ALA to PpIX; enhanced uptake of the compound resulting from impairment of the BBB surrounding glial tumors (13–15). The gene discussed is FECH; the disease is neoplasm.