Liu et al demonstrated that allergic lung inflammation exacerbates angiotensin II–induced abdominal aortic aneurysm formation in mice, whereas anti-IgE-targeted therapy suppresses AAA formation.32 Conversely, other models have suggested a protective role of eosinophils and type 2 innate cells in AAA development.33,34 One study reported that mice deficient in eosinophils exhibited fewer atherosclerotic lesions, while another study found that the absence of eosinophils had no impact on atherosclerosis development.27,35. The gene discussed is IGHE; the disease is triple-A syndrome.