A substantial body of in vivo evidence demonstrates that activation of all three PPAR subtypes—via agonists like fenofibrate (PPARα) [48–51], rosiglitazone (PPARγ) [52–55], and GW501516 (PPARβ/δ) [56, 57]—confers potent protection against endothelial dysfunction and robustly promotes reparative angiogenesis. This evidence concerns the gene PPARG and endothelial dysfunction.