TGFB1 and aneurysm: Understanding the mechanisms and consequences of this transition is complicated by the fact that in mouse models carrying germline aneurysm-causing mutations, the transition from the initial deficiency in TGF-β/Smad signaling to moderate disease and eventual overt disease is entwined with prenatal and perinatal developmental processes that regulate morphogenesis and postnatal remodeling of the aortic wall (87–89).