Given that absence of the TF cytoplasmic domain in either cardiac resident cells or bone marrow cells alleviated post-MI cardiac function and remodeling, how the TF cytoplasmic domain-PAR1-Rac1 axis and -PAR2-angionenic pathways are coordinated among specific cell types to yield the favorable outcome in TF∆CT mice needs further study. The gene discussed is RAC1; the disease is myocardial infarction.