Diclofenac is an NSAID, Non-Steroidal Anti-Inflammatory Drugs, widely used clinically in the treatement of osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis, and has been available in the United States since 1988 (Banks et al. 1995). Diclofenac can cause hepatotoxicity, and despite the rare nature of these events, affects a large number of people due to its widespread usage. It is one of the most common drugs associated with idiosyncratic hepatic injury (Daly et al. 2007). From November 1988 to June 1991 the FDA received 180 cases of diclofenac-induced adverse hepatic injury of which 79% were female, 71% were elderly patients (above the age of 60), and 77% of the patients had osteoarthritis. In most of the cases the liver injury was characterized by hepatocellular damage or mixed hepatocellular injury, and there were some cases of cholestasis (Banks et al. 1995). The incidence of diclofenac hepatotoxicity has been reported to be 6.3 per 100 000 patients (DeAbajo et al. 2004). Bioactivation to reactive intermediates, their disposition, the production of oxidative stress, mitochondrial damage, and immune-mediated mechanisms have been suggested to play a role in diclofenac-mediated liver toxicity