In addition, GLP-1R agonists have been demonstrated to affect the obesity-dependent and -independent development of hepatocellular carcinoma by acting on multiple pathways including JNK, PI3K/Akt/mTOR, and EGFR-STAT3; however, it is unknown whether GLP-1R agonist activity in hepatocellular carcinoma is due to minimizing metabolic risk factors such as obesity and insulin resistance or from genuine antineoplastic properties - or both[5]. Here, MTOR is linked to obesity due to melanocortin 4 receptor deficiency.