Specific ablation of Slc25a49 in cardiomyocytes leads to exacerbated Dox‐induced cardiomyopathy, characterized by compromised mitochondrial respiration enhanced glycolysis and increased glycolytic metabolite glucose‐6‐phosphate (G6P) levels, subsequently activating the activator protein‐1 (AP‐1) complex. This evidence concerns the gene JUNB and cardiomyopathy.