This suggests that the TTPAL-TRIP6-β-catenin axis present in disulfidptosis can activate the Wnt/β-catenin pathway, thereby promoting the progression of colon cancer.382 One study reported that,383 treating HCT116 cells with a low concentration (0.3 mM) of GYY4137 (a slow-release H2S donor) increased the proliferation rate of HCT116 cells, while enhancing mitochondrial function and glycolysis, thereby promoting tumor growth. This evidence concerns the gene TRIP6 and malignant colon neoplasm.