In line with this hypothesis we showed that the expression levels of acetylated NF-κB were significantly suppressed by AdoMet in HCT 116p53+/+ and LoVo cells and that pretreatment with AdoMet resulted in a notable decrease of acetylated NF-κB/NF-κB ratio in both 5-FU-treated cell lines, indicating that AdoMet could downregulate the expression of P-gp and reverse the MDR in CRC cells, partly at least, by suppressing the activation of the NF-κB signaling pathway. The gene discussed is NFKB1; the disease is colorectal carcinoma.