Because carcinogenesis is a multi-step process, Sporn (1976)suggested that the best time to control cancer is in its “preneoplastic" phase, before it has a chance to develop into “invasive" cancer. Therefore, the aim of the present work was to evaluate the effect of TQ on the dysplasia induced in that model, through IHC expression of both enzymes.6 weeks of DMBA painting resulted in irreversible genetic changes that did not resolve by the studied repair enzymes. So it can be proposed that TQ had resulted in regression of the carcinogenesis process through the following mechanisms. First: TQ as a potent antioxidant that antagonizes the adverse effect resulting from elevated ROS levels due to carcinogenesis i.e. reduction of the intracellular ROS allowed the repair enzymes to fulfill their main target.Second: TQ through inactivation of the TNF-Nf-κB pathway, and in turn induced p53 activation, i.e. stimulated apoptosis of malignant cells. Third: TQ has the ability to arrest cells at different phases of the cell cycle leading to growth inhibition, so allowing repair of mutated cells