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Intestinal epithelial cells constantly crosstalk with the gut microbiota and immune cells of the gut lamina propria. Enteroendocrine cells, secrete hormones, such as incretin hormones, which participate in host physiological events, such as stimulating insulin secretion, satiety, and glucose homeostasis. Interestingly, evidence suggests that the incretin pathway may influence immune cell activation. Consequently, drugs targeting the incretin hormone signaling pathway may ameliorate inflammatory diseases such as inflammatory bowel diseases, cancer, and autoimmune diseases. In this review, we discuss how these hormones may modulate two subsets of CD4 + T cells, the regulatory T cells (Treg)/Th17 axis important for gut homeostasis: thus, preventing the development and progression of inflammatory diseases. We also summarize the main experimental and clinical findings using drugs targeting the glucose‐dependent insulinotropic polypeptide (GIP) and glucagon‐like peptide (GLP-1) signaling pathways and their great impact on conditions in which the Treg/Th17 axis is disturbed such as inflammatory diseases and cancer. Understanding the role of incretin stimulation in immune cell activation and function, might contribute to new therapeutic designs for the treatment of inflammatory diseases, autoimmunity, and tumors. • CD26 blockade by vildagliptin decreased IL-17 production. • Bone marrow recipient animals from GIPR-/- donors have a decrease in Treg cells. • GLP-1 analogue (liraglutide) decreased Th17 cells and increased Treg. • Colitis-inducing mice treated with sitagliptin reduce disease status. • GLP-1R agonist (Ex-4) increased Treg population and reduce T1D. [ABSTRACT FROM AUTHOR]