Importantly, for the first time, we demonstrated that administration of both anti-FLT1 peptide and anti-FLT1 MAb increased angiogenesis, which led to an improved the pathology associated with DMD in mdx mice, and is a phenocopy of our genetic models (mdx:Cdh5-Flt1Δ/Δ mice). The gene discussed is CDH5; the disease is Duchenne muscular dystrophy.