With regards to known pathophysiological mechanisms underlying TAA onset, including aortic-wall expansion and VSMCs’ dedifferentiation from the contractile to the synthetic phenotype, which is regulated by lncRNAs’ CARMN, LUCAT1, SMILR, and MALAT1, Patamsytė and co-workers tested these molecules in clinical aortic tissue and blood-plasma samples from TAA and non-TAA patients using the qRT-PCR method [205], attributing to LUCAT1 alone the ability to discriminate aneurysmal disease in patients’ blood plasma and a diagnostic potential for TAA. The gene discussed is SMILR; the disease is Vascular dilatation.