Further analysis and Western blot validation identified the CX3CL1/GNB5/AKT2/NF-κB/apoptosis pathway as the ALL treatment mechanism in the DSS-induced IBD model, suggesting the neuroprotection effects of ALL through crosstalk of the CX3CL1–CX3CR1 axis and the neuroimmune system. This evidence concerns the gene CX3CL1 and inflammatory bowel disease.