Six out of the 17 interactions have been previously linked to invasion, migration or adhesion (EPHA4-Efnb3, SEMA5A-Plxnb3, AQP4-Dag1, FGFR1-Ncam1, FGF2-Sdc2, and APP-Aplp2) [20], [26]–[29] whereas only 3 interactions have been previously reported in glioma (SEMA5A-Plxnb3, AQP4-Dag1, and FGF2-Sdc2) [20], [26]–[31]. The gene discussed is SEMA5A; the disease is glioma.