The molecular mechanism of the effect of EET on cancer cell proliferation is achieved in part through significantly enhanced phosphorylation of the epidermal growth factor receptor (EGFR) and the activation of downstream signalling cascades, including the MAPK and PI3K/Akt pathways (Jiang et al., 2007; Nithipatikom et al., 2010). Here, AKT1 is linked to cancer.