These functional dichotomic downstream effects by TGF-β signaling in the context of GBM and normal neural cell counterparts are one of the well-known examples of the “TGF-β paradox.” Thus, we hypothesized that the Sema3A/NRP1 signaling in GBM cells and NPCs induces TGF-β pathway activation. The gene discussed is NRP1; the disease is glioblastoma.