Various methods used to overexpress VEGF such as VEGFA recombinant adeno-associated virus vectors, transplanted in vivo muscle-derived stem cells transduced for VEGFA overexpression, removal of miRNA binding sites responsible for inhibiting VEGFA translation, and antibodies binding to VEGFR-1 (VEGF Receptor 1) to increase levels of free VEGF in DMD knock-out (mdx) have all increased muscle function, fiber size, capillary density, and tissue perfusion21,27–29. Here, VEGFA is linked to Duchenne muscular dystrophy.