Men1, encoding a 610-amino acid protein named menin, is a tumor suppressor gene [1]. Mutations in Men1 lead to multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant disorder. The protein menin interacts with transcription factors and chromatin-modifying proteins in signaling pathways such as transforming growth factor β/bone morphogenetic protein, a few nuclear receptors, Wnt/β-catenin, and Hedgehog, playing a crucial role in the pathogenesis of MEN1-associated tumors [2].

Mouse models with loss-of-function mutations in the Men1 gene closely resemble the human disease in terms of tumor spectrum and associated hormonal changes, although individual tumor frequencies vary [3]. These models have been exploited for therapy-response studies testing novel drugs against neuroendocrine tumors (NETs), providing promising leads for novel therapies for MEN1-related tumors [3].

In conclusion, Men1 is essential in regulating normal physiological functions through its protein menin's involvement in various signaling pathways. The Men1-knockout mouse models have significantly contributed to understanding the role of Men1 in the development of MEN1-related endocrine and non-endocrine tumors, and have also served as a valuable research model for exploring new therapeutic strategies for these diseases.