Although other factors such as the accumulation of oxidized LDL in macrophages have been implicated in the initiation of atherosclerosis [1], [2], the data presented here may suggest an attractive alternative model, in which the dysregulation of SIRT1-AMPK-SREBP signaling and elevation of NLRP3 inflammasome components result in vascular lipid deposit and elicit inflammatory process in atherosclerosis related to diabetes (Fig. 9). This evidence concerns the gene PRKAA2 and atherosclerosis.