Our model for the mechanism of action of SF1126 in glioma cells (Figure 6D) shows that PI3-kinase can be stimulated following (1) growth factor (EGFR) mediated signals, (2) up regulated RAS signals, and/or (3) integrin (αvβ3) mediated signals, which increase the cellular levels of phospho-AKT. The gene discussed is AKT1; the disease is central nervous system cancer.