Using cardiac injury models such as myocardial infarction (MI) and thoracic aortic constriction (TAC) it was shown that fibroblast populations expand in the murine injured heart [13] and become activated effectuating a pronounced deposition of collagens and other ECM components in a process markedly orchestrated by the signaling of transforming growth factor-beta (TGFβ) [14,15], a master fibrosis regulator. The gene discussed is TGFB1; the disease is myocardial infarction.