In addition, application of the cell-permeable Cx43 carboxiterminal mimetic peptide αCT1, that competitively inhibits the interaction of endogenous Cx43 with zonula occludens-1, to cryoinjured mouse hearts was associated with reduced gap junction remodeling and lower inducibility of ventricular arrhythmias 7 to 9 days after injury [19], and decreased left ventricular volumes 8 weeks later [20]. This evidence concerns the gene GJA1 and Ventricular arrhythmia.