At genetic level, mutations in key regulatory genes, including Multiple Endocrine Neoplasia Type 1 (MEN1), Death Domain-Associated Protein 6 (DAXX), Alpha Thalassemia/Intellectual Disability Syndrome X-Linked (ATRX), and those affecting the mammalian target of the rapamycin (mTOR) signaling pathway, disrupt normal cellular mechanisms such as proliferation and apoptosis in pancreatic neuroendocrine tumors (pNETs) [6]. This evidence concerns the gene MTOR and pancreatic neuroendocrine tumor.