It has been demonstrated that COX-2 levels increase in a p53-dependent manner in response to genotoxic therapy,30 although p53 has also been shown to inhibit COX-2 gene induction.31 Our data suggest that COX-2 induction in a largely intact tumour microenvironment may also be Caspase-3 dependent, which adds further insight into the regulation of PGE2 production and β-catenin signalling during genotoxic stress in a more physiological setting. The gene discussed is CASP3; the disease is neoplasm.