PKCε activation is emerging as an important contributor to the maintenance of vascular EC homeostasis, through its ability to regulate anti-apoptotic and anti-inflammatory genes.15,16 A role for PKCε in VEGF-induced activation of Akt, Bcl-2, and eNOS, and in the protection of EC against serum starvation via modulation of eNOS activity, has also been reported.16,26,27 Moreover, when exposed to chronic hypoxia PKCε-deficient mice exhibit endothelial dysfunction, with reduced eNOS induction in pulmonary EC and increased vascular tone. Here, PRKCE is linked to endothelial dysfunction.