In myelodysplastic syndromes, for example, Rac activation is impaired in neutrophils and CD34+ progenitors [30], accompanied by impaired lipid raft formation and a corresponding reduction in the generation of reactive oxygen species after fMLP stimulation in granulocyte-macrophage colony-stimulating factor primed neutrophils [31]. The gene discussed is AKT1; the disease is myelodysplastic syndrome.