Indeed our studies showed that in VWF-deficient EC in vitro, release of Ang-2 was increased.4 More recent preliminary data from BOEC confirmed these observations, since Ang-2 release from type 1 and type 3 VWD patients was found to be increased compared to control (Starke, Randi et al, in preparation). The gene discussed is ANGPT2; the disease is von Willebrand disease 3.