Previously, we found that overexpression in the mouse liver of a myristoylated/activated form of AKT1 (myr-AKT1 with C-terminal HA tag), which will be here referred to as AKT, leads to extensive hepatic steatosis and increased expression of enzymes of the lipogenic pathway, such as FASN, ACAC, ACLY, and SCD1 [19]. The gene discussed is AKT1; the disease is steatosis.