In the present study, we found that the administration of FGFR4 inhibitors, on one hand, can significantly inhibit the HCC cell growth via suppressing the downstream PI3K/AKT pathways (Fig. 3I), and on the other hand, may result in the accumulation of EZH2 by activating the non-canonical NF-kB signaling transcription factor NFKB2 (Fig. 1J-N), leading to the failure of Roblitinib to eliminate tumor cells (Fig. 1B and 2B-F). Here, PIK3CB is linked to neoplasm.