Zhaoyue He and Hans-Uwe Simon*; Institute of Pharmacology; University of Bern; Bern, Switzerland;* Email: hus@ pki. unibe. ch; http://dx. doi. org/10.4161/cc. 23418 not in p53-negative cells. Downregulation of NCF2 with siRNA-based approach results in reduced ROs production and increased cell death in HCT 116 and HaCat cells. This suggests that NOX2 expression is a sort of ROsdependent cell survival factor owing to the influence of ROs on p53 (Fig. 1). it should be mentioned, however, that high ROs concentrations can also kill cells. 5 Taken together, these results provide a new insight into the network of p53 and ROs production. since p53 can act both pro-and anti-apoptotically, the pro-oxidant NCF2/p67phox can thus support the anti-apoptotic role of p53 under certain conditions. in this case, p53 is probably required to maintain a sufficient level of NCF2/p67phox for cell survival. However, under which circumstances p53 activates NOX2 and how they modulate the cell fate are still questions of interest at the moment. in summary, the identification of NCF2/p67phox as a novel target of p53 extends our understanding of the partnership between p53 and ROs production and further highlights the unknown role of p53 in inflammatory diseases, such as cardiovascular, autoimmune