Finally we evaluated the phenotypic activity of DRAK2 in cell systems. We suspected DRAK2 expression was already significantly suppressed in HCA7 cells, given high levels of COX-2 expression whereas HT-29 cells showed lower levels of COX-2 with higher levels of DRAK2 expression. Following transient transfection of HT-29 cells with a commercially available sequence validated siRNA to DRAK2, significant repression of DRAK2 transcription was seen ( Figure 5A ). To counteract the effects of low transfection efficiency and maximise detection of a phenotype associated with DRAK2 silencing, a GFP expression vector was cotransfected to 'gate'-transfected or 'silenced' cells in subsequent assays to quantify cell survival using an established method (Vezina et al, 2001) . The percentage of viable cells (without 7-ADD uptake) and non-viable cells (with 7-ADD uptake) was calculated in mock-transfected cells and in DRAK2 siRNA-transfected cells selected (gated) by GFP fluorescence. Loss of cell viability was observed in mock-transfected HT-29 cells following treatment with both SC236 and staurosporine ( Figure 5B ). In contrast, the siRNA-transfected (GFP-gated) cells showed no loss of cell viability following treatment with the COX-2 inhibitor SC236. They did however still show a significant loss of viability with staurosporine, suggesting a specific effect on the pathway involved in the action of SC236.