Consequently, in combination with epigenomic changes that also selectively target negative regulators of Ras upstream of PI3K-Akt and Wnt antagonists, we hypothesized that the PI3K-Akt and Wnt pathways functioned collectively to activate clonal expansion of EBV-infected cells in HDs and EBVaGCs and promoted the tumor evolution (Fig. 7c). This evidence concerns the gene AKT1 and neoplasm.