In mitochondria, KAT8 binds to mtDNA through KANSL3,stimulating the expression of mitochondrial genes involved in oxidativephosphorylation, with KAT8 catalytic activity being essential for thisfunction[241].Deletion of KAT8 in the heart and skeletal muscle using muscle creatine kinase(MCK) promoter-driven Cre recombinase leads to mitochondrial degeneration anddysfunction of oxidative phosphorylation in cardiomyocytes, resulting inhypertrophic cardiomyopathy and heart failure in mice. The gene discussed is KAT8; the disease is cardiomyopathy.