Importantly, the anti-inflammatory effects of EA were significantly attenuated in the SDV+EA group, confirming that vagal integrity is essential for EA to fully exert its suppressive action on these key inflammatory pathways and mediators.<h4>Conclusion</h4>EA ameliorates FD by modulating vagal nerve activity, concurrently suppressing TWEAK/Fn14/NF-κB pathway activation and arachidonic acid metabolism, thus attenuating duodenal low-grade inflammation in FD model rats. The gene discussed is TNFRSF12A; the disease is Fabry disease.