The AHR: Adaptive evolution or one-off?

In this issue of Blood, Belghasem et al have expanded the territory in our search for pathogenetic factors in cancer-associated venous thromboembolism (VTE).¹ Such factors, which could potentially be used as biomarkers or therapeutic targets, are usually elusive when chased and ephemeral when caught. Time has not been kind to many of the previously identified factors, from D-dimers to tissue factor (TF)-bearing microparticles² and it will be interesting to see whether the hypothesis that the vascular endothelial cell (EC) aryl hydrocarbon receptor (AHR) contributes to the development of cancer-associated venous thrombosis withstands the test of time.