A STAT3 inhibitor attenuated angiotensin II-induced AAA progression in mice through inhibiting vascular inflammation and maintaining autophagy (35), whereas severe angiotensin II-induced AAAs were noted in mice overexpressing SOCS3, another negative regulator of JAK2/STAT3 signaling, in T lymphocytes in association with impaired IL-17 production (34). The gene discussed is SOCS3; the disease is achalasia-alacrima syndrome.