Furthermore, the depletion of p65 dramatically increased the apoptosis rates of doxorubicin-exposed HCC cells, suggesting that NF-κB activation impairs the chemosensitivity of tumor cells and the inhibition of NF-κB signaling represents an effective strategy to overcome the chemoresistance of HCC to doxorubicin. Here, NFKB1 is linked to neoplasm.