Rivaroxaban improved cardiac systolic function in the MI mouse model and reduced infarct size and cardiac mass by downregulating the mRNA expression of PAR-1 and PAR-2, as well as TGF-β and tumor necrosis factor-α (TNF-α) in the infarcted area, and of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the non-infarcted area [87]. The gene discussed is TGFB1; the disease is myocardial infarction.