Transcriptomics studies in aortas from Marfan syndrome mouse models (Fbn1C10341G/+) [10] and multi-omics approaches in human aortas from MFS patients [101,102] have consistently revealed significant reductions in key regulators of mitochondrial function, including PGC1α, TFAM, and mitochondrial complexes. Here, TFAM is linked to Marfan syndrome.