In a follow-up research, Sun et al. performed functional analyses on the Q49X mutant and proved that the mutation disturbed the intracellular distribution and the cell-to-cell electrical coupling of gap junctions and also impaired the localization of both wild-type Cx40 and Cx43 to the cell-to-cell interfaces, which might be the pathogenesis of AF in the family [72]. The gene discussed is GJA5; the disease is atrial fibrillation.