Given the frequent activation of both RAS/MAPK and PI3K/AKT/mTOR pathways in almost 50% of HCC patients21, to examine whether chemotherapy would enrich for CD133+ tumor-initiating/propagating cells in HCC, flow cytometry analysis for CD133 expression was carried out on a hydrodynamic tail vein injected (HTVI) NRasV12+Myr-AKT proto-oncogenes-driven HCC mouse model that was treated either with DMSO control or 5-FU or cisplatin. This evidence concerns the gene AKT1 and neoplasm.