In this context, the fact that enforced expression of fat-1 in 3T3-L1 preadipocytes restored the mTORC1 activity elevated by APC depletion and that DHA treatment inhibited adipogenic differentiation of 3T3-L1 preadipocytes potentiated by APC depletion, collectively suggesting a possible role of increasing n-3/n-6 ratio in the suppression of mTORC1 activation induced by APC depletion and the consequent adipogenesis and lipemia. The gene discussed is APC; the disease is hyperlipidemia.