Unlike previous reports reaching the similar result of significantly reduced colitis-associated cancer in fat-1 TG mice [13, 14], our study is quite novel in revealing the following three cancer preventive mechanisms: blocking of the dissociation of β-catenin to inhibit β-catenin-driven abnormal proliferation, significant induction of tumor suppressive 15-PGDH, and determination of an advisable dietary dose of exogenous ω-3 PUFAs to achieve CAC prevention in clinic. This evidence concerns the gene FAT1 and neoplasm.