Interestingly, Ntn1−/− Mø mice were less susceptible to AAA when challenged to control AAV in the presence of Ang II and only 20% that received PCSK9 AAV in conjunction with Ang II developed features of AAA, as depicted in the macroscopic images of the renal region of the aorta (Fig. 3i). This evidence concerns the gene NTN1 and triple-A syndrome.