MEN1 encodes menin, a nuclear scaffold protein that functions as a tumor suppressor primarily through its role in transcriptional regulation and chr11 modification 1. Menin is an essential component of histone methyltransferase complexes that regulate gene expression, particularly affecting endocrine tissue development and function. Loss-of-function mutations in MEN1 cause multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant cancer predisposition syndrome characterized by parathyroid hyperplasia, pancreatic islet tumors, and pituitary adenomas 2. The protein demonstrates biallelic inactivation in approximately 30% of certain endocrine tumors including parathyroid adenomas, gastrinomas, and insulinomas, but only 1-5% of common pituitary tumors 3. MEN1-associated tumors typically exhibit more aggressive behavior, larger size, earlier onset, and greater treatment resistance compared to sporadic counterparts 45. While menin primarily functions as a tumor suppressor in neuroendocrine tissues, recent evidence indicates it can also promote tumorigenesis in certain cancer types, demonstrating context-dependent dual functionality 1. The syndrome significantly reduces life expectancy, with patients dying at a mean age of 55 years, primarily from malignant pancreatic endocrine tumors and thymic carcinoids 6.