von Willebrand factor (vWF) is a key glycoprotein primarily expressed in endothelial cells and stored in Weibel-Palade bodies, playing a vital role in hemostasis and vascular biology (1). It is also present in platelets and the subendothelial matrix, contributing to thrombosis and inflammation (2). vWF expression is heterogeneous in different tissues, for example, in the kidney, its expression varies among glomerular endothelial cells, affecting susceptibility to complement-mediated injury in atypical hemolytic uremic syndrome (aHUS) (2). In the brain, vWF is abundant in endothelial cells and contributes to blood-brain barrier regulation, affecting permeability under hypoxia and seizures (3). Disease associations include von Willebrand disease (vWD), thrombotic thrombocytopenic purpura (TTP), and cardiovascular disorders. In vWD, impaired vWF leads to bleeding tendencies, while excessive vWF activity in TTP causes microvascular thrombosis (2). Additionally, vWF modulates angiogenesis by regulating endothelial cell proliferation and migration (1).