Actually, oxidative stress occurs when organisms encounter reactive oxygen species such as superoxide anion, hydrogen peroxide and hydroxyl radical. ROS are known to be produced during the oxidative burst of professional phagocytes to kill intracellular bacteria during an infection. Therefore, in phagocytic cells, bacteria have to cop with a stressful and hostile environment in which multi-drug and stress resistance mechanisms can confer a selective advantage for intracellular survival in the host. The exact role of TolC in response to oxidative stress is still unclear, but it could participate in the efflux of toxic ROS in addition to ROS degradation by the Oncrasin-1 bacterial periplasmic and cytoplasmic catalases and dismutases. Moreover, in E. coli, tolC belongs to the marA/soxS/rob regulon including over 40 genes that promote resistance to multiple antibiotics and to superoxides. Four tolC promoters have been described in E. coli, suggesting the involvement of multiple transcriptional regulatory elements in response to different environments. We show here that p73 acts as a T cell-specific tumor suppressor in a genetically defined mouse model, and that concomitant ablation of p53 and p73 predisposes mice to an increased incidence of thymic tumors compared to the loss of p53 alone. Our results demonstrate a causal role for loss of p73 in progression of T cell lymphomas to the stage of aggressive, disseminated disease. We provide evidence that tumorigenesis in mice lacking p53 and p73 proceeds through mechanisms involving altered patterns of gene expression, defects in early T cell development at the Atractyloside A immature DN2-DN4 stage, impaired apoptosis, and the ensuing accumulation of chromosomal aberrations, i.e. chromosome gains, losses, and clonal translocations. We further demonstrate that p73 loss alone cannot initiate tumorigenesis but it can cooperate with an initiating lesion, such as p53 loss-of-function, to make a premalignant cell tumorigenic and proliferatively aggressive. There are two current concepts of the cellular mechanisms responsible for the induction and maintenance of T cell lymphomas.