The late deterioration of allografts remains a problem despite improvements in short-term and long-term graft survival. The previous concept that late deterioration reflects a specific disease -- chronic rejection -- is being replaced. The new view is that many factors are involved in late deterioration, including the age and pretransplant condition of the organ, injury from brain death, injury from the transplant process, T cell-mediated and antibody-mediated rejection (in some cases reflecting poor compliance with immunosuppressive drugs) and post-transplant organ-specific stresses in the new environment, including drug toxicity, infectious agents, hypertension and lipids. Ultimately these stresses interact with the intrinsic limitations in repair and homeostasis in the tissues of the organ, producing characteristic syndromes. The most important recent advance has been the emergence of potent immunosuppressive drug combinations that have greatly reduced rejection.