Reactive oxygen species (ROS) can serve as intracellular signals that promote cell proliferation and survival at sub-toxic levels, or function as toxic substances that cause cell death and senescence at high levels (Weinberg and Chandel, 2009). p53 plays a key role in the control of cellular response to ROS by upregulating the expression of either antioxidant genes under low level of oxidative stresses or pro-oxidative and apoptotic genes under high level of stresses (Vigneron and Vousden, 2010; Hafsi and Hainaut, 2011). However, how p53 differentially regulates gene expression in response to different ROS level remains elusive. Δ133p53 is an N-terminal truncated form of p53 (Bourdon et al., 2005) and functions to antagonize p53 apoptotic activity and to promote DNA double-strand break repair (Chen et al., 2009; Aoubala et al., 2011; Gong et al., 2015). In this study, we investigated the functional interaction between p53 and Δ133p53 in response to various levels of ROS.