In conclusion, using both transgenic mice and cellular models, we have shown that (1) stable elevation of n−3/n−6 ratio via transgenic expression of fat-1 prevent colorectal carcinogenesis associated with APC mutation and alleviate the accompanying anemia and rectal relapse; (2) the inhibition of mTORC1 by increased n−3/n−6 ratio is associated both with the suppression of CRC development itself and with the rebalance of lipid metabolism associated with CRC. The gene discussed is FAT1; the disease is colorectal carcinoma.