Moreover, exogenous Sema3A, which is thought to signal in ECs via Nrp1 and PlexinA1/A4, was also found to trigger the apoptosis of aberrant and immature blood vessels in cancer (Maione et al, 2009); intriguingly, the data suggested that Sema3A might promote vessel normalization also by recruiting SMCs (Fig 1), a mechanism that was not observed by Yang et al (2015) for Sema3C. The gene discussed is SEMA3C; the disease is cancer.