Atherosclerosis, also known as hardening of the arteries, is a condition where an artery wall thickens as a result of buildup of cholesterol or plaque. It is a major cause of death and disability in the United States, accounting for approximately 50% of all deaths in adults. According to the World Health Organization (WHO), ischemic heart disease (atherosclerosis affecting the arteries that supply blood to the heart) and stroke (atherosclerosis affecting the arteries to the brain) are the world’s biggest killers, accounting for a combined 15.2 million deaths in 2016. Although previous studies involving twin, siblings and families have demonstrated the heritability of atherosclerosis, many specific genes causing atherosclerosis are still unknown. Our research involves generation of new genetic crosses of mice to identify quantitative trait loci (QTL) for atherosclerosis, and the difference in phenotypes between many mouse strains. Our lab identified a major QTL on mouse chromosome 17 affecting atherosclerotic lesion size. Mep1a is a promising candidate gene for the QTL. We use Mep1a knockout mice to define the influence of this gene on carotid atherosclerosis. Female mice were fed on a Western diet for 12 weeks and I am in the process of sectioning carotid artery samples. Cryosections collected will be stained with oil red O to visualize atherosclerotic lesions. I will do immunohistochemical analysis to assess cellular components of the lesions and perform morphologic measurements of atherosclerosis. Differences in two inbred mouse strains; B6 and C3H, will be presented along with the measurements of the lesion size.