Notwithstanding, a number of our experiments support a direct effector role for alloantibody in the development of late parenchymal injury and allograft vasculopathy: allograft histology revealing clear evidence of humoral, but a lack of overt cellular, rejection; the association of alloantibody production and endothelial complement deposition; Akt signaling induced in allogeneic endothelial cells by exposure to sera from transplanted mice; and restoration of rejection by passive transfer of alloantibody into T and B cell deficient Rag2−/− recipients [see also (4)]. The gene discussed is AKT1; the disease is vascular disorder.