Cyclosporin A (CsA); an immunosuppressive agent, is broadly used for the remedy of autoimmune diseases and after organ transplantations. However, its medical and experimental use is restrained with the aid of quite few side effects, such as nephrotoxicity, cardiotoxicity, hypertension and hepatotoxicity. Despite its toxicity, CsA remains to be one of the most usually used immunosuppressive agent due to its therapeutic efficacy. The key mechanisms involved in organ damage caused by CsA include altered redox homeostasis and chronic systemic inflammation. Indeed, various mechanisms have been suggested for CsA induced hepatotoxicity along with the development of reactive oxygen species, oxidative stress, and hepatic antioxidant system depletion. In some of the side findings, many mechanisms concerned have been appreciably explored and explained. Nevertheless, the mechanisms underlying CsA-mediated hepatotoxicity are not utterly understood. This review discusses CsA toxicity and its pathophysiology and role of oxidative stress in the initiation of the toxicity in addition to the different Therapeutic approaches for its toxicity.