As shown in Figure 1C, increased AKT phosphorylation was observed in cells with enforced expression of mutant P85α under both high and low serum culture conditions, thus confirming that these P85α mutants were able to drive increased signaling through the PI3K pathway independent of upstream, serum-induced, signaling events in GBM-relevant cellular contexts. This evidence concerns the gene AKT1 and glioblastoma.