The results revealed that METTL17 deficiency suppressed tumor progression, as Mettl17+/− mice exhibited benign adenoma with well-differentiated glandular tubular structures and diffuse cytoplasmic distribution of β-Catenin, while WT mice displayed malignant tumors with hypo-differentiated carcinoma and nuclear localization of β-Catenin (Fig. 3K). This evidence concerns the gene METTL17 and cancer.