We observed an upregulation of HDAC6 expression in the left atria of mice at 2 weeks post‐MI, accompanied by atrial enlargement, increased atrial fibrosis and inflammation, myocyte hypertrophy, impaired mitochondrial biogenesis, elevated levels of Wnt3a, GSK3β, and β‐catenin protein, and reduced gap junction CX43 expression; these alterations were reversed by HDAC6 deletion. This evidence concerns the gene HDAC6 and myocardial infarction.