Consequently, this results in a significant decrease in the AF precursor acetyl-CoA, (2) the disruption of the redox system, subsequently activating antioxidant enzymes which are considered key elements in the regulation of AF-related genes, and (3) the disruption of fungal cell wall biosynthesis, ergosterol biosynthesis, and ATPase [63]. This evidence concerns the gene DNAH8 and atrial fibrillation.