INSM2 is a transcriptional repressor that plays critical roles in neuroendocrine development and metabolic homeostasis. As a member of the Snail/Gfi1/Insm1 superfamily 1, INSM2 expression is directly regulated by the transcription factors Neurogenin3 and NeuroD1 in pancreatic islet cells 1. In pancreatic beta cells, INSM2 is essential for glucose-stimulated insulin secretion; Insm2-deficient mice exhibit elevated fasting glucose, reduced insulin secretion, and impaired glucose tolerance, with compensatory upregulation of the homologous gene Insm1 2. Beyond pancreatic function, INSM2 regulates hepatic lipid metabolism through control of the ultraconserved RNA uc.372, which suppresses miR-195/miR-4668 maturation to modulate lipogenic gene expression including ACC, FAS, SCD1, and CD36 3. In neuroendocrine tissues, INSM2 integrates into differentiation cascades downstream of Ngn3/NeuroD1 signaling 1. Clinically, INSM2 emerges as a biomarker in Alzheimer's disease, where it regulates energy metabolism-related genes 4, and in thyroid cancer, where it contributes to radioactive iodine therapy response prediction 5. These findings establish INSM2 as a multifunctional transcriptional regulator bridging neuroendocrine differentiation, glucose metabolism, and energy homeostasis.