Its migration from polar ends to lateral surface of the cell is linked to abnormal cardiomyocyte-to-myofibroblast coupling and the associated risk of arrhythmia; for this reason, Cx43 has been proposed as a potential target for prevention of aberrant cardiomyocyte coupling and myofibroblast proliferation in the infarct border zone [44]. This evidence concerns the gene GJA1 and cardiac arrhythmia.