AXIN1 and neoplasm: The abnormal excitation of the pathway involved accumulation of β-catenin in the cytoplasm affected by the reduced stability of the upstream GSK3-β-related β-catenin destruction complex, and then stimulation of the T cell factor/lymphocyte enhancer factor (TCF/LEF) to regulate Wnt responsive downstream target oncogene expression, including Axin1, c-Myc, and CyclinD1, which can lead to cell proliferation, inhibition of cell apoptosis, and tumor formation [37].