So far, our results demonstrated that oral administration of the S6K1 inhibitor LY in mice following a HFD regime (a) dampens fat expansion and hypertriglyceridemia, while (b) downregulating a number of molecular cascades in adipose — including adipogenesis, mTORC1 signaling, and inflammation — and (c) modulates the hepatic response to high amounts of fatty acids, such as the activation of key gene nodes related to PIK3/AKT/mTOR signaling and protection against steatosis. The gene discussed is AKT1; the disease is hypertriglyceridemia.