Because colon cancer cells co-expressing mut-p53 and truncated version of APC, such as SW480 cells, do not possess a functional β-catenin degradation complex, we reasoned that the inhibition of GSK-3β by its phosphorylation at Ser 9 observed in a null-p53 H1299 cell line expressing mut-p53 cannot affect the β-catenin levels in colon cancer SW480 cells, and thus, another mechanism must exist in these cells to explain how mutant p53 can stimulate β-catenin-mediated transcriptional activity. The gene discussed is GSK3B; the disease is malignant colon neoplasm.