Their study further provided evidence that TGFβ mediates upregulation of FAP expression in U87 glioma cells through the canonical Smad-dependent TGFβ signaling pathway, in which activated TGFβ receptor induces phosphorylation of Smad (pSmad) and pSmad further directly activates transcription of the FAP gene by binding to its promoter (Figure 1a). The gene discussed is FAP; the disease is central nervous system cancer.