In this study, we used wild‐type (HDAC6+/+) mice, HDAC6 knockout (HDAC6−/−) mice and Tubastatin A (TubA, known as a potent and highly selective HDAC6 inhibitor16) to investigate the role(s) of HDAC6 in post‐MI cardiac remodelling and dysfunction, focusing on the TGF‐β1/Smad2/3 signalling pathway. This evidence concerns the gene TGFB1 and myocardial infarction.