Accordingly, we hypothesized that Tie2, one of the upstream signalling mediators of the PI3K/Akt/eNOS pathway, might be activated by aliskiren and might subsequently regulate the PI3K/Akt/eNOS pathway, thus leading to an increase in the in vitro function and in vivo reendothelialization capability of EPCs in patients with hypertension. The gene discussed is AKT1; the disease is hypertensive disorder.