Interestingly, 3MA treatment reduced apoptotic cell death in Akap1-/- mice after MI (Fig 4B and 4C), and although it increased myocardial fibrosis in the same group (Fig 4D), it significantly improved cardiac dysfunction in Akap1-/- mice one week after MI, as shown by a significant increase in % fractional shortening (Fig 4E). The gene discussed is AKAP1; the disease is myocardial infarction.