In the current study, CD38 deficiency in SMCs significantly reversed the AngII-induced decreases in the expression of contractile marker proteins such as α-SMA, SM22α, and MYH11 and the upregulation of the expression of the synthetic marker protein Vimentin in the aorta of the AAA animal model, indicating that CD38 participated in the phenotype switch from a contractile phenotype to a synthetic phenotype. This evidence concerns the gene VIM and triple-A syndrome.