Vascular smooth muscle cell (VSMC) accumulation is a hallmark of atherosclerosis,1 and VSMCs also generate the bulk of the neointima formed after vessel occlusion or injury.2–4 VSMCs display remarkable phenotypic plasticity in vitro,5 and lineage-tracing experiments have convincingly shown that VSMC phenotypic switching occurs in vivo.3,4,6–9 Healthy, mature VSMCs are quiescent and express contractile genes, such as alpha smooth muscle actin (aSma) and smooth muscle myosin heavy chain (SMMHC/Myh11). Here, ACTA1 is linked to atherosclerosis.