Mechanistically, immunoprecipitation and confocal microscopy analyses showed that integrin α5β1 activated by TNIIIA2 both physically and functionally cooperated with PDGF-stimulated PDGF-Rβ and, consequently, PDGF-Rβ was hyperactivated, which led to the stimulation of Ras-MAPK and Akt signaling pathways (rat glioma C6 cells: Figure 3C, human GBM T98G cells and rat glioma 9L cells: Ref. The gene discussed is PDGFRB; the disease is glioblastoma.