When the levels of full-length Cx43 protein are markedly reduced via an M213L mutation associated with an absence of GJA1-20k which is an auxiliary subunit for the trafficking of Cx43, the abnormal propagation of electrical impulse, including decrease in R wave amplitude, elongation of QRS complex duration, and increase in frequency of premature ventricular contractions (PVC), occurred in rats undergoing the loss of Cx43 gap junction that contributes to arrhythmias [75,76]. This evidence concerns the gene GJA1 and Arrhythmia.