Interestingly, and in sharp contrast with ischemic HF, FTO inhibition appears to be therapeutic in hyperlipidemia- and palmitic acid (PA)-induced cardiomyopathy and cardiomyocyte inflammation, respectively, where its targeted pharmacological inhibition by a LuHui monomer derivative was reported to provide therapeutic benefit, likely via disrupted mRNA translation of cluster of differentiation 36 (CD36), alias scavenger receptor class B protein (SR-B2).154. Here, FTO is linked to cardiomyopathy.