Mice with targeted inactivation of TGF-β1 in their megakaryocytes and platelets are partially protected from developing cardiac hypertrophy, fibrosis, and systolic dysfunction in a pressure overload transverse aortic constriction model,22 and are partially protected from AS progression in a murine hypercholesterolemic model (low-density lipoprotein receptor [LDLR]−/− apolipoprotein [Apo]B100; LA100) in which mice spontaneously develop AS.22 Here, APOB is linked to aortic stenosis.