NF-κB has a key role as a pivotal link between inflammation and cancer.23 Recently, NF-κB inhibitors have been severed as a new target for tumor therapy.24,25 Numerous studies displayed that MTs had been shown to interact with NF-κB and mediated its antiapoptotic effects.18,19 In this study, we demonstrated that knockdown of endogenous MT1X led to downregulation of p-IκB-α and cyclinD1 but induced IκB-α upregulation, which was in line with the typical apoptosis of AML cells resulting from regression of NF-κB activation. This evidence concerns the gene CCND1 and neoplasm.