The anti-atherosclerosis and attenuated plaque formation effects of GLP-1 RAs are mediated through inhibiting the overall inflammatory response by suppressing the expression and release of proinflammatory cytokines (such as interleukin-6 and tumor necrosis factor-α) and suppressing the activation of nuclear factor-kappa B signaling pathway (23, 24). This evidence concerns the gene GLP1R and atherosclerosis.