Previous reports of this animal model have described: hepatic damage (increased blood levels of alanine aminotransferase and aspartate aminotransferase), histopathological changes in the liver, alterations in brain biochemical parameters (increase in neuronal nitric oxide synthase, NADPH oxidase activity, over-activation of glucose-6-phosphate dehydrogenase, and a decline in phosphofructokinase-2), and behavioral abnormalities characteristic of Type C HE [36,39,40,41]. The gene discussed is FMO5; the disease is hereditary elliptocytosis.