Overall, our observations of increased hypomethylation, larger tumor size, activation of PI3K/AKT/mTOR, EGFR, Wnt, and Ras pathways, and downregulation of p53 pathway upon IDH1 R132Q expression supports these findings, suggesting that the R132Q mutation somehow confers features reminiscent of more aggressive, typically non-IDH1-driven tumors through mechanisms not likely directly involving CpG hypermethylation. The gene discussed is AKT1; the disease is neoplasm.