Interestingly, the activation of cardiomyocyte Krüppel-like factor-5 (a factor which regulates cardiac fatty acid metabolism via the direct activation of peroxisome proliferator-activated receptor) is found in HF patients and mice with ischemic cardiomyopathy, associated with increased Cer biosynthesis; the genetic (deletion of KLF5 gene) or pharmacological (ML264) inhibition of KLF5 in AMI mice prevents Cer accumulation, reduces cardiac remodeling, and improves the ejection fraction [101]. This evidence concerns the gene KLF5 and ischemic cardiomyopathy.