Intriguingly, IL-18 upregulated a set of genes that are collectively thought to serve as markers of pro-inflammatory cell phenotype (CCL2, IL-6, VCAM-1, Galectin3, TNF-α and OLR1; Figure 4), while downregulating SMC marker genes (ACTA2, MYH11; Figure 4), suggesting that IL-18 promotes the phenotypic modulation of ASMC to an atherosclerosis-promoting inflammatory phenotype. Here, ACTA2 is linked to atherosclerosis.