Anti-oxidant defense is known to be regulated by various mechanisms including the usage of nuclear factor erythroid 2-related factor 2 (Nrf2). Under normal physiological conditions, Nrf2 is bound to Kelch-like ECH-associated protein 1 (Keap1), a cytoplasmic repressor. Keap1 also acts as a substrate adaptor for Cullin3-dependent ubiquitin ligase and also targets Nrf2 for degradation by proteosomes. The substrate adaptor function of Keap1 is inactivated during physiological stress. In this respective condition, a range of oxidative and electrophilic stimuli such as ROS, diethyl malonate, and certain disease processes, resulting from Nrf2 accumulation, enters the nucleus and thereby activates the expression of select anti-oxidant genes. Such genes promote the detoxification of ROS and other harmful molecules, which contribute to the carcinogenesis.