The human gene RHAG encodes a Rhesus blood group family type A glycoprotein which is expressed specifically in erythroid cells. It is thought to mediate ammonium export from these cells (Marini et al. 2000, Westhoff et al. 2002). Defects in RHAG are the cause of regulator type Rh-null hemolytic anemia (RHN, Rh-deficiency syndrome). RHN is a form of chronic hemolytic anemia (Hyland et al. 1998).