Several mechanisms have been proposed, including the expression level of CD33 on blasts and the frequency of CD33-positive blasts (57–61); CD33 expression on non-AML blood cells acting as a sink for GO (62); P-glycoprotein transporter activity in AML blasts (58); CD33 splice variants and polymorphisms (63); and other mechanisms (52, 64, 65). This evidence concerns the gene CD33 and acute myeloid leukemia.