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). This evidence concerns the gene FGF19 and liver cancer.