Cells can undergo cell-cycle arrest to repair damaged DNA or apoptosis to eliminate permanently damaged cells that carry inaccurate genetic information following genotoxic stresses.The two cell fates are determined by signaling cascades that seem to converge on p53 signaling.However, how thresholds of p53 activation are intricately controlled by orchestration of increasingly many factors remains unclear.Here we show that Axin, a central regulator of Wnt signaling, forms distinct complexes with Pirh2 and Tip60 as well as HIPK2 and p53 at their endogenous levels,during different cellular commitments.