In an elastase‐induced mouse model of AAA, researchers mimicked the SOCS1 kinase inhibitory structural domain with a synthetic cell permeable‐peptide (S1) to inhibit STAT activation, and found that the S1 peptide inhibited aortic M1 macrophages while promoting the expression of M2 macrophages‐associated markers, and downregulating the pro‐inflammatory cytokines. The gene discussed is SOCS1; the disease is triple-A syndrome.