As elucidated previously (Fu et al., 2016), knockdown/knockout of Sam68 substantially sensitizes human colon cancer cells to undergo spontaneous apoptosis and retards colon tumor development in Apcmin716/+ mice, which highlights the critical role of Sam68-dependent NF-κB transactivation in the cellular responses to the intrinsic DNA damage that occurs frequently in the rapidly-dividing/proliferating cancer cells. This evidence concerns the gene KHDRBS1 and malignant colon neoplasm.