demonstrated that the deletion of AKT1 conferred protection against the development and progression of chronic hypoxic pulmonary hypertension, and played a dominant role in pulmonary vascular remodeling.[44] Specifically, AKT1 might be involved in glycolytic shift and metabolic reprogramming, as well as endothelial dysfunction mediated by various factors including PHD2 and AIP1.[45, 46] In the present study, we mainly focused on the activation of the PI3K/AKT pathway by S100A9 via its receptor RAGE, and its role in modulating endothelial cell function. The gene discussed is S100A9; the disease is endothelial dysfunction.