Thus, we assessed (1) whether NAC administration after infarction modulates Cx43 expression and attenuates ventricular arrhythmias, and (2) whether NAC-induced Cx43 changes are PKA or Epac dependent in a rat MI model by the use of inhibitors of PKA, Epac and adenylate cyclase as well as the measurement of cyclic nucleotides. The gene discussed is GJA1; the disease is myocardial infarction.