For instance, it was shown that the re‐expression of the N‐terminal proteolytic fragment of Histone Deacetylase 4 (HDAC4‐NT) under high O‐GlcNAc conditions can serve as a preventive measure against HDAC4‐dependent DCM, whereas mice lacking HDAC4 (HDAC4‐KO) develop HF.38 This evidence concerns the gene HDAC4 and familial dilated cardiomyopathy.