Previous animal studies have shown that tVNS suppressed atrial fibrillation by down-regulating both c-fos and NGF and by preventing the loss of atrial connexins (Cx40 and Cx43), an essential component of gap junctions and a key player in the formation of AF substrate, which suggests that tVNS suppresses autonomic remodeling by modulating cardiac autonomic nervous system (Chen et al., 2015; Yu et al., 2017b). Here, GJA5 is linked to atrial fibrillation.