The proposed mechanism linking MEN1 mutations with tumor formation involves disruption of the interactions between menin and other proteins, such as activating protein-1 (AP-1), transcription factor Jun D or nuclear factor-κB (NF-κB) to suppress Jun-mediated or NF-κB-mediated transcriptional activation, and between members of the Smad family, Smad3 and the Smad 1/5 complex, ultimately resulting in modified cell cycle regulation and proliferation (13,14). The gene discussed is JUN; the disease is neoplasm.