AKT1 and neoplasm: Considering the functional enrichment of differentially expressed genes, our findings converge on a model whereby the genetic alterations such as CNVs that accumulate during turn or invasion lead to loss of differentiated astrocyte properties and gain of known features driving tumor aggressiveness, angiogenesis, dedifferentiation and oncogenic PI3K/AKT signaling (Fig. 4H), ultimately resulting in the promotion of glioma progression towards more aggressive and invasive phenotypes.