STAT3 and neoplasm: In hepatocellular carcinoma models induced by DEN combined with either high-fat/high-carbohydrate or low-fat/low-carbohydrate diets, lean m/db mice, and MCD- or CDE-induced liver injury—as well as in human models, exenatide activation of the GLP-1R–cAMP–PKA–EGFR–STAT3 pathway suppressed oncogenic signaling, limited tumor cell growth, and enhanced apoptosis, resulting in a marked reduction in tumor progression (Zhou et al., 2017).