Thyroid cancer cells express Gal-3,23,33,40,41 a beta-galactoside-binding lectin, which associates with the development and malignancy of many types of tumors.42 Overexpression of Gal-3 promotes neoplastic transformation by interacting with K-Ras-GTP, enhancing K-Ras-GTP anchorage to the cell membrane, and enabling it to activate downstream signal pathways.5 In the present study, we found that combined treatment with FTS and MCP significantly decreased K-Ras and Gal-3 expression. This evidence concerns the gene KRAS and thyroid cancer.