NFKB1 and neoplasm: We observed that CBX6suppression caused decreases in ERK1/2 phosphorylation and MAPK-p38, NF-κB-p50, and NF-κB-p65 phosphorylation and thatCBX6overexpression increased ERK1/2 phosphorylation and MAPK-p38,NF-κB-p50, and NF-kB-p65 phosphorylation, indicating that CBX6may mediate tumor progression in HCC cells by promoting cellular proliferation, which is linked to the MAPK and NF-κB signaling pathways.