The anti-neoplastic properties of these agents result from the inhibition of prostaglandin generation, particularly that of prostaglandin E 2 (PGE 2 ), the most abundant in vivo product of COX-2 activity in CRC cells (Pugh and Thomas, 1994; Rigas et al, 1993) . Although it appears that PGE 2 modulates various processes that are fundamental to tumour cell survival, such as altered proliferation and susceptibility to apoptosis (Sheng et al, 1997 (Sheng et al, , 1998 (Sheng et al, , 2001 Tang et al, 2002) , the precise molecular mechanisms remain unclear. A strong rationale exists therefore to generate a more complete understanding of the downstream targets of COX-2 activity (Doherty and Murray, 2009 ). This may lead to the development of more refined therapies, with side-effect profiles that allow their generalised use. Previous studies examining gene regulation by COX-2 in CRC cells have focused on long time points and have used relatively high doses of NSAIDs (Zhang and DuBois, 2001) . With this in mind, we set out to explore early changes in gene expression in CRC cells resulting from low-dose treatment with a selective COX-2 inhibitor, to improve our understanding of the early signalling events downstream of prostaglandin production. One candidate gene that we have identified, DRAK2 (DAP kinase-related apoptosis-inducing kinase 2 or STK17b), is one of a family of serine threonine kinases that share the ability to induce apoptosis (Sanjo et al, 1998) . The aim of this study was to explore the relationship between COX-2 and DRAK2 as a potential downstream regulator of cell survival in CRC. 