Evidence that MMF suppresses the production of anti-HLA antibodies, inhibits the recruitment of mononuclear cells into the allograft, as well as the proliferation of arterial smooth muscle cells, has been taken to suggest that MMF might play an important protective effect against the development and progression of CAN. Thus, an immunosuppressive regimen based on low-dose MMF as sole antirejection drug not only would avoid chronic toxicity of steroids, and calcineurin inhibitors, but would also limit the risk of CAN, the main cause of allograft loss in the long-term. On the other hand, however, the Mycophenolate Steroid Sparing (MYSS) trial found that AZA was as effective as MMF in preventing acute allograft rejection in CsA-treated kidney transplant recipients, even after steroid withdrawal. Since acute allograft rejection is one of the strongest predictor of CAN, these findings can be taken to suggest that, in the long-term, AZA might share with MMF also a similar protective effect against the development of CAN. Moreover, it must be emphasized that chronic CsA nephrotoxicity is a major component of CAN. Thus, the prevalence and severity of CAN may be reduced in patients on CsA-free immunosuppressive regimens. In this clinical setting, the benefits of MMF against the development of CAN might not appreciably exceed those of AZA. Should this be the case, AZA might confer the same benefits of MMF, but at remarkably lower costs since, at equivalent doses, AZA is about 15 times less expensive than MMF.