Several mechanisms of resistance to anti-angiogenic treatments have been identified.3 Amongst them, the compensatory activation of the angiopoietin/Tie-2 axis has been proposed as one of the main drivers of resistance.4 We have previously shown that elevated angiopoietin-2 (Ang2) levels counteract the therapeutic effects of bev in colorectal cancer patients5 and that the combined inhibition of both VEGF and Ang2 improved tumour growth control and vascular normalisation.6 These findings confirmed Ang2 as a promising anti-angiogenic target in conjunction with VEGF-targeting therapy. This evidence concerns the gene TEK and colorectal cancer.