The oral administration of GABA or the GABAA-R agonist homotaurine inhibits autoreactive Th1 and Th17 cells while promoting CD4+ and CD8+ Treg responses [10,11,13], ameliorates autoimmune disease in mouse models of type 1 diabetes (T1D), multiple sclerosis, and rheumatoid arthritis, and also limits inflammation in murine type 2 diabetes [3,10,11,14,15]. Here, CD4 is linked to type 1 diabetes mellitus.