The tumor-inhibiting effects of Ex-4 were in accordance both in GLP-1R-abundant HCC cell lines and in a xenograft mouse model, wherein both PKA and EGFR had a significant contribution in Ex-4 functions, while Ex-4 treatment led to arrest of cell growth and inhibition of EGFR signaling in both HepG2 and Huh7 cells. The gene discussed is GLP1R; the disease is hepatocellular carcinoma.