A total of five candidate genes were obtained, including Pim1, Jdp2, Zfp36, Cd38 and Parp14. Currently, studies have reported that the expression level of CD38 is positively correlated with the diameter of the abdominal aorta and that the lack of CD38 in SMCs can inhibit the progression of AAA (38, 39). The gene discussed is PARP14; the disease is triple-A syndrome.