GM-CSF neutralization abrogated inflammatory aneurysm development and matrix-degrading activity in a Smad3−/− mouse model.58 Clinically, a positive correlation between plasma concentrations of GM-CSF and intracranial aneurysms has been reported,60 and circulating levels of GM-CSF are also elevated in patients with acute aortic dissection.59 All of this evidence supports the concept that GM-CSF plays a major part in atherosclerosis and AAAs, in part by sustaining miR-181b levels. Here, SMAD3 is linked to achalasia-alacrima syndrome.