The results support our previous proposal (Végh and Papp, 2011) that in arrhythmia point of view the modification of GJ function, for example, by preventing the ischemia-induced dephosphorylation of Cx43, would particularly be important during that “critical” phase of ischemia when the rate of uncoupling of GJs rapidly increases, and when other factors, implicated in arrhythmogenesis, are also present. Here, GJA1 is linked to ischemia.