In addition to acting through the p38 pathway, GLP-1RAs also promote the increase of PKA levels via the cAMP-dependent pathway, which in turn prevents the phosphorylation of epidermal growth factor receptor (EGFR) and activator of transcription 3 (STAT3), resulting in the inactivation of the EGFR-STAT3 signaling pathway in tumor cells and subsequently downregulating several downstream effector genes such as myelocytomatosis oncogene (c-Myc), survivin, cyclin D1, Bcl-xl, and Bcl-2, thereby inducing apoptosis in tumor cells in a dose-dependent manner [70, 73]. This evidence concerns the gene BCL2 and neoplasm.