Vion et al. reported that low shear stress-mediated AMPK downregulation of autophagy plays a key part in the onset and progression of atherosclerosis due to (1) establishing a pro-inflammatory EC phenotype following downstream inhibition of KLF2 and ICAM-1 upregulation (Figure 4, left panel), (2) increased EC apoptosis following an increase in the apoptosis regulator p53 and (3) increased EC senescence mediated by elevated levels of p16 [87]. This evidence concerns the gene PRKAA2 and atherosclerosis.