FLT1 and neoplasm: For example, computational modeling has predicted that tumor endothelial cells overexpressing membrane VEGFR1 contribute to the therapeutic resistance to anti-VEGF-A treatment because the VEGF-A ligands captured by membrane VEGFR1 can dissociate to increase free VEGF-A levels in tumors, counteracting the anti-VEGF-A treatment (Weddell and Imoukhuede, 2014).