The present study demonstrates the importance of activating FcγR in antibody‐mediated responses during AAA formation: (i) FcγR isoforms are expressed in human and experimental AAA; (ii) blockade of activating FcγR signaling by γ‐chain gene deficiency or Syk kinase inhibition limits AAA development in mice; and (iii) these protective effects associate with changes in chemokines (CCL2/5 and CXCL10), cytokines (TNFα, IFNγ, and IL‐17/10), redox enzymes (NOX1/2/4, catalase, and SOD1) and matrix degrading enzymes (MMP2/9), and phenotypic modulation of VSMC and macrophages. Here, IL17A is linked to triple-A syndrome.