We have confirmed that DRAK2 expression in colon cancer cells in vitro is regulated by COX-2 ( Figure 2 ) and also demonstrated an in vivo relationship between COX-2 and DRAK2 expression in human CRC (Figure 3 ). Both COX-2 and DRAK2 have been implicated in the modulation of T-lymphocyte function, with opposing phenotypic consequences. Activated T cells in patients with SLE markedly upregulate and sustain COX-2 expression and resist inactivation and cell death (Xu et al, 2004) . Indeed, COX-2 expression has been shown to mediate lethal T-cell activation (Brewer et al, 2003) . By contrast, over-expression of DRAK2 in activated T cells enhances apoptosis in the presence of IL-2 (Mao et al, 2006) , and studies in mice with targeted disruption of DRAK2 have demonstrated that this protein is an important negative regulator of T-cell activation, raising the threshold for activation through the T-cell receptor (McGargill et al, 2004; Friedrich et al, 2005) and acting as an important regulator of T cells response and survival (Schaumburg et al, 2007; McGargill et al, 2008) .