We hypothesize that EA attenuates NLRP3 inflammasome activation, engages the efferent fibers of the vagus nerve, initiates the cholinergic anti‐inflammatory pathway, conveys signals to intestinal neurons, suppresses IL‐1β/IL‐18 secretion, and ultimately downregulates tryptophan metabolism, contributing to the attenuation of IBD. This evidence concerns the gene NLRP3 and inflammatory bowel disease.