Consistently, our data also indicate that the blockade of the FGF19/FGFR4 pathway by small molecules (i.e. irreversible FGFR4 inhibitors), which is currently being evaluated in clinical trials,43 cannot further exacerbate the inhibitory effect induced by EIF4A3‐silencing, thus showing that the main actions exerted by EIF4A3 in the modulation of HCC aggressiveness are mediated by the controlling of FGFR4 splicing. Here, EIF4A3 is linked to hepatocellular carcinoma.