Further studies have reported that linc-CCAT2-rich glioma-cell-derived SEVs can be taken up by HUVEC cells and can increase the expression level of linc-CCAT2 in HUVEC cells in turn promoting HUVEC migration, proliferation, tubular formation in vitro, and small artery formation in vivo and inhibits hypoxia-induced HUVEC cell apoptosis. The gene discussed is CCAT2; the disease is glioma.