SEMA3A and neoplasm: In fact, when overexpressed at much greater than physiological levels through adeno-associated virus (AAV) vectors, Sema3A has been found to inhibit angiogenesis both by similarly overexpressed VEGF in AAV-treated muscles (Zacchigna et al, 2008) and by lower endogenous VEGF levels in tumor models (Maione et al, 2009, 2012).