Our discovery that acidosis exerts marked control over HMBG1 and Bcl2 expression as well as downstream inflammation responders and Akt, via miR-126 and HIF-1α (summarized in Figure 6), in the context of chronic ischemia is novel and represents important additions to our understanding of vascular inflammation and cell survival during ischemic disease, including atherosclerosis and vasculatures of solid tumors, wherein hypoxia and acidosis are integral disease components. This evidence concerns the gene AKT1 and ischemic disease.