As the most therapeutically relevant aspect of targeting ACLY lies in the ability to dedifferentiate activated myofibroblasts to a less fibrotic phenotype, we tested the translational potential of ACLY-mediated myofibroblast reversion in human CFs isolated from HF donors diagnosed with non-ischemic cardiomyopathy (NICM). This evidence concerns the gene ACLY and ischemic cardiomyopathy.