There is an ongoing debate about the anatomical origin of the neointimal cells that are responsible for venous stenotic lesions in arteriovenous fistulas. Liang and co-workers show that vascular smooth muscle cells from the feeding artery contribute substantially to venous intimal hyperplasia in a murine AVF model. In addition, they show that increased Notch signaling is the driving force behind FSP-1-mediated migration of these cells to the venous outflow tract.