For instance, HO-1 and its by-products play a protective role against the progression of atherosclerosis through the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB activation), which results in the attenuation of tumor necrosis factor (TNF)-α-induced upregulation of vascular cell adhesion molecule 1 (VCAM-1) and E-selectin in endothelial cells (ECs) and in the decreased expression of TNF-α, interleukin (IL)-1β, and macrophage inflammatory protein-1β in macrophages (Wu et al., 2011; Barbagallo et al., 2013; Cheng et al., 2014; Fredenburgh et al., 2015). This evidence concerns the gene VCAM1 and atherosclerosis.