SMAD3-deficient fibroblasts exhibit reduced migratory potential, and reduced potential for transdifferentiation, that is consistent with a reduction in α-smooth muscle actin expressing myofibroblasts with reduced contractile function in SMAD3-deficient hearts after myocardial infarction (Dobaczewski et al., 2010). The gene discussed is SMAD3; the disease is myocardial infarction.