Specifically, liraglutide’s effect in pre-established atherosclerosis has been studied in vivo in ApoE−/− mice and ex vivo in human atherosclerotic plaques, with the results indicating the drug’s ability to reduce M1 proinflammatory mediators, such as MCP-1, TNF-a, and IL-1b, and upregulate the cathepsin protein family in the bone marrow, leading to an attenuation of atherosclerosis in the aorta through an increase in M2-like macrophages [160]. The gene discussed is CTSS; the disease is atherosclerosis.