Of note, this study also showed that reconstitution of CD28−/− mice with wild-type Tregs protected the mice from the development and rupture of AAA, providing direct evidence that impaired Treg function, but not modulation of Teff immune responses, is a central mechanism for the exacerbation of AAA formation under the condition of the CD80/CD86-CD28 pathway blockade. This evidence concerns the gene CD86 and triple-A syndrome.