PTEN-uating restenosis.

Within the last few years, the lipid phosphatase PTEN has gained increasing attention.1 Initially described as a tumor suppressor gene, the function of PTEN meanwhile ranges from the regulation of the immune system to the recently established important function in neuronal growth.1,2 On a cellular level, PTEN interferes with cell proliferation, survival, and growth. These effects are not restricted to a certain cell type or species but have been demonstrated from Drosophila to humans and in various cell types including cardiomyocytes.2–4 Consistent with a crucial role for PTEN in the regulation of cell fate, the complete deficiency of PTEN leads to embryonic lethality in mice.5,6 On a molecular level, PTEN dephosphorylates phosphatidylinositol(3,4,5) trisphosphate [PtdIns (3,4,5)P3], which is formed by the phosphatidylinositol-3-kinase (PI3K).4 Thereby, PTEN antagonizes the diverse downstream signaling effector pathways activated by PI3K-derived phospholipids (Figure).