The identification of Nrp1 as a modulator of Alk1 signalling output, and the striking normalization of the hypervascular phenotype in Alk1-deficient retinas by deletion of a single copy of Nrp1 raises the prospect that targeting Nrp1 activity could provide treatment options for Hereditary Haemorrhagic Telangiectasia (HHT) patients carrying inactivating Alk1 mutations58. The gene discussed is ALK; the disease is hereditary hemorrhagic telangiectasia.