The aim of this study was to investigate the curative effect of AMY on atherosclerosis and its anti-inflammatory role in ApoE−/− mice and BMDMs, particularly its association with mitogen-activated protein kinases (MAPKs), activator protein-1 (AP-1) and nuclear factor-kappa B (NF-κB) p65 signaling pathways. The gene discussed is FOS; the disease is atherosclerosis.