MYT1 is a multifunctional zinc-binding transcription factor with distinct roles in neuronal development and cell cycle regulation. In the central nervous system, MYT1 functions as a DNA-binding transcription factor that regulates proteolipid protein genes and controls oligodendrocyte development 1. MYT1 safeguards neuronal identity by actively repressing non-neuronal lineage programs through recruitment of Sin3b-containing repressor complexes, while maintaining neuronal gene expression and silencing developmental pathways like Notch signaling 2. Beyond its transcriptional role, MYT1 also functions as a membrane-associated protein kinase (PKMYT1) that regulates the G2/M cell-cycle checkpoint 3. This kinase activity is essential for cell survival under genotoxic stress by controlling the transition from G2 phase to mitosis, allowing time for DNA repair 4. In pancreatic β-cells, MYT1 and its family member MYT3 regulate insulin secretion and cell survival under metabolic stress, with variants associated with Type 2 diabetes 5. Clinically, MYT1 inhibition represents a therapeutic vulnerability in cancer cells dependent on G2/M checkpoint control, showing synergy with DNA-damaging chemotherapies and checkpoint inhibitors 134. Additionally, MYT1 mutations have been identified in hemifacial microsomia, a congenital craniofacial malformation 6.