Specifically, oxidative stress may contribute to gap junction abnormalities seen in obesity by slowing forward trafficking and causing hyperphosphorylation of connexin 43, as discussed previously, altering conduction through resultant gap junctions, resulting in conduction slowing (Lin et al., 2006; Smyth et al., 2010; Gemel et al., 2017). This evidence concerns the gene GJA1 and obesity due to melanocortin 4 receptor deficiency.