Several studies on tissue samples from mouse models and MFS patients have identified promising target genes that could prevent the deterioration of aortic aneurysms, such as Tfam, which is crucial for mitochondrial respiration, and miR-632, which is involved in Wnt/β-catenin signaling, End-Mt, and fibrosis, as well as miR-122, associated with the inflammatory response. The gene discussed is TFAM; the disease is Marfan syndrome.