It has been well documented that in both treatment by doxorubicin (Dox), a genotoxic anticancer drug, and in Dox-resistant cancer cells, the ubiquitination system is activated [25,26,27] leading to either enhancement of the activation of NF-κB by promoting degradation of the inhibitor IκBα [28] or activation of the DNA damage repair system [29] resulting in reduced Dox sensitivity. This evidence concerns the gene NFKB1 and cancer.