The silencing (and the overexpression) of HDAC6 respectively decreased (and increased) mitochondrial oxidative stress production and pyroptosis, accompanied by negative (and positive) modulations of the Wnt3a/GSK3β signaling pathway in HL1 cells under oxidative stress conditions, providing evidence of a potential mechanistic explanation of an HDAC6‐mediated Wnt3a/GSK3β signaling pathway in the modulation of the atrial fibrosis and remodeling in post‐MI mice under our experimental conditions. The gene discussed is HDAC6; the disease is myocardial infarction.