Furthermore, we demonstrated that the EIF4A3‐dependent inclusion of exon 2 in FGFR4 is essential to mediate the signalling of FGF19 and the maintaining of the FGF19/FGFR4 axis in HCC, in that EIF4A3‐silencing not only reduced the basal phosphorylation levels of downstream pathways associated to FGF19/FGFR4, including GSK3β(Ser9), ERK(Thr202/Tyr204), AKT(Ser473) and SRC(Y419) (Figure 6F), but also blunted the FGF19‐induced phosphorylation of GSK3β, ERK, AKT and SRC in liver cancer cells (Figure 6F). The gene discussed is AKT1; the disease is liver cancer.