CEND1 (cell cycle exit and neuronal differentiation 1) is a transmembrane protein that serves as a crucial regulator of neuronal differentiation and cell cycle exit. The protein promotes neuronal differentiation by directly reprogramming glial cells into induced neurons, with overexpression in human cortical astrocytes leading to GABAergic neuronal identity and upregulation of neuronal genes while downregulating astrocytic markers 1. Mechanistically, CEND1 functions through mitochondrial regulation, forming dimers via conserved GXXXA motifs in its transmembrane domain to enhance ATP synthesis through interaction with ATP synthase subunit Atp5f1b 2. The protein acts as a tumor suppressor in cardiac regeneration, where LSD1-dependent suppression of CEND1 is essential for cardiomyocyte proliferation and heart repair after injury 3. Clinically, CEND1 shows significant disease relevance across multiple conditions. Elevated plasma CEND1 levels serve as an early biomarker for Alzheimer's disease risk, appearing 15 years before diagnosis and progressively increasing 4. In Parkinson's disease, CEND1 expression is markedly downregulated, and the protein exerts neuroprotective effects by suppressing NF-κB pathway activation, reducing apoptosis and inflammatory responses 5. CEND1 also shows prognostic value in gliomas, where high expression correlates with better survival and enhanced immune infiltration 6.