Although it is clear that DRAK2-mediated cell death is cell-type and context dependent, there is a growing body of evidence to indicate that its function is directly related to the regulation of cell survival. In addition to in vivo evidence from DRAK2 transgenic mice (Mao et al, 2006) , induction of DRAK2 in vitro in a variety of contexts and cell types augments apoptosis (Sanjo et al, 1998; Kuwahara et al, 2006; Mao et al, 2006) . We also show that silencing DRAK2 expression in HT29 cells promotes cell survival and abrogates the effects of a COX-2 inhibitor in vitro. These findings confirm published observations on the effect of DRAK2 silencing by RNAi on susceptibility of rat colon cancer cells to UV-induced apoptosis (Kuwahara et al, 2006) . We also recently observed that DRAK2 may be important in the ability of COX-2 to protect cardiomyocytes from doxorubicin-induced apoptosis (Neilan et al, 2006) , suggesting that the modulation of DRAK2 expression may not be confined to cancer but may also be important in the positive effects of COX-2 on cell viability and tissue healing in other systems. For the moment, the precise mechanisms by which DRAK2 impacts on cell survival are unclear. Recent observations suggest that the ribosomal kinase p70S6, involved in cell-cycle regulation, is a substrate for DRAK2 (Mao et al, 2009) , highlighting a possible involvement in regulation of cell-cycle dynamics. In an analysis of publicly available expression data (Whitfield et al, 2002) , we have noted that DRAK2 forms part of a cluster of genes showing similar cyclical changes in expression with cell-cycle periodicity in HeLa cells (Supplementary Figure S3 ; Supplementary Table 2 ). There is an interesting degree of overlap (summarised concisely in Supplementary Figure 4) between this panel and COX-2-regulated genes identified by our gene expression analysis and a number of other gene discovery studies that examined the effects of COX inhibitors (Iizaka et al, 2002; Levitt et al, 2004) .