These new findings, in conjunction with our prior discovery that ethanol supplementation to AD elevates the expression of the gap junction channel Gja1 mRNA [14], contributing to an augmented risk of lethal arrhythmias during the lethal arrhythmia-evoked test, underscore the crucial roles played by MASH-related LV MIF and the upregulation of Gja1 mRNA expression in the development of lethal arrhythmias. This evidence concerns the gene GJA1 and Alzheimer disease.