Arteriovenous malformations (AVMs) are direct connections between arteries and veins that arise during active angiogenesis. Most AVMs are sporadic but some are associated with mutations in genes involved in TGFβ signalling. For example, mutations in activin receptor-like kinase 1 (ALK1, a TGFβ receptor) are implicated in the vascular disorder hereditary haemorrhagic telangiectasia 2 (HHT2). But what are the molecular and cellular errors that lead to AVM formation? On p. 1573 Beth Roman and colleagues address this question by analysing AVM development in alk1 mutant zebrafish embryos. They report that blood flow triggers alk1 expression in nascent arteries exposed to high haemodynamic forces and that Alk1 normally limits vessel calibre. In alk1 mutants, however, Alk1-dependent arteries are enlarged, and the downstream vessels adapt to the consequent increases in blood flow by retaining normally transient arteriovenous drainage connections, which subsequently enlarge to form AVMs. This two-step model for AVM formation suggests that HHT2 treatments might focus on preventing arterial enlargement and/or abrogating flow-induced AVM development.