Indeed, dabigatran was shown to antagonize growth, cell-cycle progression, migration, and endothelial tube formation induced by thrombin in the invasive breast cancer cell line expressing high levels of protease-activated receptor 1 (PAR-1) (Vianello et al., 2016) that was, most probably, the result of p53 mutation (Salah et al., 2008). The gene discussed is F2R; the disease is invasive breast carcinoma.