FN1 and cardiac hypertrophy: Because the genetic model non-selectively ablates fibronectin in most somatic cells, the exact source of fibronectin remains elusive, although a more recent study, by inducibly abolishing fibronectin specifically in fibroblasts, suggests fibroblast-derived fibronectin as a major driver for cardiac hypertrophy and fibrosis after ischemic injury [86].