Furthermore, mRNA levels of TGF-β target genes (ID1, ID3, and LIF) in GBM cells were significantly increased by rSema3A, and this induction was abolished in NRP1-knockdown GBM cells, suggesting that NRP1 is a main effector molecule in Sema3A-induced TGF-β signaling activation (Figure 4B). This evidence concerns the gene SEMA3A and glioblastoma.