Experimentally, we demonstrated that in the absence of p53, GSK3B activity allows cells to survive, despite treatment with DNA-damaging drugs, by sustaining DNA repair and that its downregulation restored sensitivity to 5-FU of p53-null colon cancer cells - both in in vitro and in in vivo models - via induction of regulated necrosis[48]. This evidence concerns the gene TP53 and colonic neoplasm.