Wang et al. (2011) reported that increased TMAO levels enforced macrophages to accumulate cholesterol by inducing SR-A1 as a scavenger receptor. In addition, Mohammadi et al. (2016) showed that TMAO-induced upregulation of SR-A1 at mRNA and protein levels, contributed to the development of ER stress as well as lipid-laden macrophage activation in atherosclerosis (Hotamisligil, 2010). This evidence concerns the gene SRA1 and atherosclerosis.