Since the U87 glioma cells and the AZVU001A glioma stem-like cells were sensitive and fully resistant, respectively, to TGFbeta-1-mediated upregulation of FAP enzymatic activity (Figure 4A,B), we wondered whether this difference may be due to the absence of activation of the canonical TGFbeta receptor/Smad signaling pathway in the glioma stem-like cells. The gene discussed is FAP; the disease is glioma.