FAK is the link between integrins and downstream signaling transduction pathways and activates ERK and PI3K/AKT pathways involved in cell proliferation and migration (19); short term cilengitide treatment inhibited the FAK/Src/AKT-dependent pathway in endothelial and glioma cells but did not affect ERK activation in HUVEC cells (20). The gene discussed is AKT1; the disease is central nervous system cancer.