Indeed, Nar inhibited the phosphorylation of IκB, an upstream mediator of NF-κB function, and thus, p65 localization into nuclear was also inhibited in colorectal and breast cancer cells treated with Nar (Figure 4a, b), supporting the involvement of NF-κB inactivation in Nar-induced apoptosis. This evidence concerns the gene CPSF4 and breast carcinoma.