Consistent with this hypothesis, Kaminska and co-workers reported that glioma-derived soluble factors induce the activation of focal adhesion kinase, PI3K (phosphoinositide 3-kinase)/Akt (protein kinase B), ERK (extracellular-signal-regulated kinase), and P38 MAPK (mitogen-activated protein kinase) signaling pathways, resulting in enhancement of cell motility, phagocytosis, sustained proliferation and a distinct genomic response. The gene discussed is AKT1; the disease is central nervous system cancer.