Elucidation of the phosphatidylinositol metabolism to control steatohepatitis and hepatocellular carcinoma

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Deletion of phosphatidylinositol 3 kinase isozymes such as p110α, p110γ, and p110δ did not inhibit development of hepatic lesions in Pten KO mice. Inpp4 is a phosphatase which dephosphorylates PI(3, 4)P2 that is metabolite of PI(3, 4, 5)P3 and has the same function as PI(3, 4, 5)P3, a substrate of Pten. We made clear that Inpp4 or Akt2 and PPARγ, downstream molecules of Pten, played a critical role in development of hepatic lesions in Pten KO mice.