Despite the pronounced attenuation of AngII-infusion AAA formation in mice with whole body TLR4 deficiency, repopulation with TLR4-deficient bone marrow-derived cells in lethally irradiated LDLR-deficient mice exhibited no effects on AAA formation, suggesting that TLR4 exerted its action on AAA through non-hematopoietic cells [22]. The gene discussed is TLR4; the disease is triple-A syndrome.