Under physiological conditions, Ang-1 is constitutively expressed at higher concentrations than Ang-2 [18]; however, during pathological conditions (due to inflammation, ischemia/hypoxia or hyperglycemia) preformed Ang-2 is released from Weibel–Palade bodies of endothelial cells, provoking an increased Ang-2/Ang-1 ratio and a disruptive effect on vascular stability [19]. The gene discussed is ANGPT2; the disease is Hyperglycemia.