In this study, we showed that (1) 60% of ccRCC specimens harboured an FGFR4 copy number amplification; (2) FGFR4 copy number correlated with FGFR4 protein expression; (3) FGFR4 inhibition suppressed intracellular signalling pathways, including ERK1/2, Akt/mTOR, and STAT3 pathways; (4) the selective FGFR4 inhibitor BLU9931 suppressed tumour growth, leading to apoptotic cell death in vitro; and (5) BLU9931 treatment shrunk tumours in ccRCC xenograft mice. This evidence concerns the gene AKT1 and neoplasm.