To further determine whether NF-κB is the central signaling pathway by which RBBP6 promotes the EMT process in CRC, we treated the RKO-RBBP6 cells with exogenous IκBα-M (IκBα dominant-negative mutant, which can block NF-κB activation but cannot be ubiquitinated and degraded by proteasome) or NF-κB inhibitor BAY11-7082, and treated the HT29-sh-RBBP6 cells with plasmid expressing p65 which can promote the activation of NF-κB pathway. The gene discussed is NFKB1; the disease is colorectal carcinoma.