UV light–induced angiogenesis was reported many years ago by Bielenberg et al. [37], who demonstrated increased endothelial cell proliferation (bromodeoxyuridine + CD31 + cells) within existing blood vessels, leading to telangiectasia and new blood vessel development in mice skin due to a UV radiation–induced imbalance between a positive angiogenic molecule (basic fibroblast growth factor) and a negative angiogenic molecule (interferon-beta). The gene discussed is FGF2; the disease is Telangiectasia.