Nevertheless, any remaining increases in hepatic lipogenesis may continue to be supported by elevations in activities of hepatic IRS-2/PI3K and aPKC, which we found to be well maintained, even when diabetes is produced by experimental destruction of insulin-producing pancreatic islet cells [12,22] Whether other factors, e.g., conventional or novel PKCs (cPKCs or nPKCs), that activate S6 kinase are needed to substitute for Akt in maintaining hepatic lipogenesis in later stages of T2DM is uncertain. This evidence concerns the gene INS and type 2 diabetes mellitus.