On the other hand, LSS or OSS could increase the secretion of proinflammatory mediators such as C-reactive protein, IL-6, GRO-a (or CXCL1), and IP-10 (or CXCL10) in atherosclerotic plaques [120, 121], which could induce M1 macrophage polarization through increasing the expression of RelA (p65 subunit of NF-κB) and c-Jun N-terminal kinase [122] and activate inflammatory mediators in atherosclerosis [123]. This evidence concerns the gene NFKB1 and atherosclerosis.