Depletion of DCs can inhibit AAA growth.[33] Although the exact role of different monocyte subsets in AAA remains incompletely understood, AAA lesions contain both CD11b+Ly6Chi and CD11b+Ly6Clo monocytes.[34] We recently reported a protective role of EOS in angiotensin‐II (Ang‐II) infusion‐induced AAA in mice.[11] Therefore, the increase of pro‐inflammatory neutrophils, DCs, and CD11b+Ly6Chi monocytes, but decrease of anti‐inflammatory EOS and CD11b+Ly6Clo monocytes, may result from increased AAA growth due to loss of ILC2. This evidence concerns the gene ITGAM and triple-A syndrome.