Moreover, SESN2-knockdown mice had higher plasma pro-inflammatory cytokine levels and increased monocyte recruitment to the vascular endothelium by secreting monocyte adhesion molecules [intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1] through inhibiting the AMPK signaling pathway and downregulating the ER stress pathway, which contributed to atherosclerosis initiation (32). This evidence concerns the gene SESN2 and atherosclerosis.