The ventricular lumen area, as a measure of ventricular dilatation, was comparable in the two control groups and in the AngII-treated PAR2-deficient mice, and only in the AngII-treated wt mice was the ventricular lumen significantly increased by 1.7-fold compared with the AngII-treated PAR2-deficient animals (Fig 1C). The gene discussed is F2RL1; the disease is Vascular dilatation.