Rhesus (Rh) blood group antigens consist of several membrane-associated polypeptides including RHAG, which is required for cell-surface expression of the complex. The Rh(null) phenotype arises from missing or severely deficient Rh antigens and sufferers present a clinical syndrome of varying severity characterised by abnormalities of red cell shape, cation transport and membrane phospholipid organisation. The human gene RHAG encodes a Rhesus blood group family type A glycoprotein (belonging to the SLC42 solute transporter family) which is expressed specifically in erythroid cells. A transport function for RHAG is suggested to mediate ammonium (NH4+) export from these cells and prevent toxic build-up of NH3/NH4+ (Westhoff et al. 2002, Ripoche et al. 2004). 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 (Huang & Ye 2010).