Metastatic PNETs and cervical carcinomas are transformed into benign lesions by re-expressing SEMA3A, since SEMA3A not only enhanced cancer tissue oxygenation and increased the normalization window to inhibit sunitinib-induced activation of epithelial–mesenchymal transition (EMT) and hypoxia-dependent signaling pathways, such as the hypoxia-inducible factor 1-α related pathway, but also prevented tumor hypoxia and restrained cancer dissemination [45]. This evidence concerns the gene SEMA3A and neoplasm.