Since the incidence of AAA is low in the absence of hypercholesterolemia28 and in order to increase the susceptibility of normocholesterolemic Ntn1−/−Mø and WTMø C57BL/6 mice to AAA, we injected the mice with a single dose of an adeno-associated virus (AAV) vector expressing the D374Y gain-of-function proprotein convertase subtilisin/kexin type 9 (PCSK9) that resulted in sustained hypercholesterolemia, as described previously29. Here, PCSK9 is linked to triple-A syndrome.