AKT1 and neoplasm: PPARγ pro-angiogenic effects are associatedwith the induction of VEGF and increased phosphorylation of eNOS and AKT [7, 75], which cause elevated VEGFproduction in human and rodent VSMCs, MΦs and tumor cells [76–79], VEGF and VEGFR levels in theECs and myofibroblasts [80].