LGALS3BP and atherosclerosis: Finally, we detected the expression of Lgals3bp in the human aorta, plasma‐derived EVs, and found that compared with healthy individuals, the expression of Lgals3bp was up‐regulated in EVs derived from the plasma of patients with MAFLD (Figure 10K), and that the protein levels of Lgals3bp were elevated in human atherosclerotic lesions (Figure 10L), consistent with previous reports.[43] Collectively, these data suggest that Lgals3bp‐rich EVs potentially serve to promote atherosclerosis and calcification.