In vitro (astrocytes exposed to ammonia) and animal models of HE show Alzheimer type II astrocytosis as the characteristic pathological lesion in HE, thought to result from mild swelling caused by the osmotic effects of intra-cytosolic glutamine (Gregorios et al. 1985, Norenberg 1987), as well as other ammonia-related changes related to glial fibrillary acidic protein (Bélanger et al. 2002) and peripheral type benzodiazepine receptors (Lavoie et al. 1990). The gene discussed is GFAP; the disease is hereditary elliptocytosis.