To unveil the implication of FGFR4 splicing in the functional role of EIF4A3 in HCC, we performed a rescue assay overexpressing the full‐length FGFR4 receptor (which is a FGFR4 version not susceptible to be processed through splicing as long as it does not contain introns) in EIF4A3‐silenced cells (HepG2 and Hep3B; Figure 7A). This evidence concerns the gene EIF4A3 and hepatocellular carcinoma.