O‐GlcNAcylation stabilized c‐Myc and thus increased its transcriptional activity, consequently activating the foetal gene program to induce cardiac hypertrophy.83 Sp1, a transcription factor involved in the development of myocardial hypertrophy, has multiple O‐GlcNAcylation sites.84 It has also been shown that insulin‐induced O‐GlcNAcylation of Sp1 triggers its nuclear translocation where it is partially or wholly deglycosylated, then phosphorylated to activate foetal gene expression.85 Here, INS is linked to cardiac hypertrophy.