Our earlier studies demonstrated a cardiovascular reparative role for eosinophil-derived IL4 and IL13 in myocardial infarcted hearts, pressure overload-induced cardiac hypertrophy, and angiotensin-II infusion-induced AAA.16–18 Yet, adoptive transfer studies showed that donor eosinophils from wild-type (WT), Il4−/− or Il13−/− mice did not differ in reversing the atherosclerotic findings in Apoe−/−ΔdblGATA recipient mice. The gene discussed is IL4; the disease is triple-A syndrome.