However, the underlying molecular mechanism remained unclear.[21] Our global gene expression analyses demonstrated that key oncogenic pathways in hepatocarcinogenesis involved in cell proliferation and survival, e.g. PI3K/AKT/mTOR, MAPK/ERK, IGF-1, as well as Nrf2-mediated oxidative and xenobiotic stress response are significantly regulated by the EGb761 treatment in hepatoma cells (Fig 5 and Table 1). This evidence concerns the gene AKT1 and hepatocellular carcinoma.