Systemic inhibition of either thrombin or PAR1 attenuated atherosclerosis progression and even promoted features of plaque stability, due to effects on endothelial function, proinflammatory signalling and immune cell infiltration.41,45–48 Thus, cell type specific deletion of PAR-1 is needed to directly assess VSMC-specific effects in disease and, specifically, fibrous cap formation in atherosclerosis lesions. The gene discussed is F2R; the disease is atherosclerosis.