To elucidate the role of IRF8‐expressing cDC1s in the AAA microenvironment, we utilized Batf3−/− mice, which lack cDC1s throughout the body.[18] These mice exhibited phenotypes similar to those observed in models with Irf8 depletion (Figure 3E,F; and Figure S3C, Supporting Information), suggesting that cDC1 acts as the cellular mediator of IRF8 function during AAA development. Here, MPPE1 is linked to triple-A syndrome.