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For example, chemotherapeutics which overrun the first obstacle of redox\u2010regulated cellular uptake channels (MDR1, MDR2, and MDR3) induce a concerted action of phase I\/II metabolic enzymes with a temporal redox\u2010regulated axis. This results in rapid metabolic transformation and elimination of a toxin. This metabolic axis is tightly interconnected with the inducible Nrf2\u2010linked pathway, a key switch\u2010on mechanism for upregulation of endogenous antioxidant enzymes and detoxifying systems. As a result, chemotherapeutics and cytotoxic by\u2010products of their metabolism (ROS, hydroperoxides, and aldehydes) are inactivated and MDR occurs. On the other hand, tumour cells are capable of mounting an adaptive antioxidant response against ROS produced by chemotherapeutics and host immune cells. The multiple redox\u2010dependent mechanisms involved in MDR prompted suggesting redox\u2010active drugs (antioxidants and prooxidants) or inhibitors of inducible antioxidant defence as a novel approach to diminish MDR. 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