ZNF292 is a highly conserved zinc finger transcription factor critical for neurodevelopment and transcriptional regulation. The protein functions as a DNA-binding transcription factor that regulates RNA polymerase II-dependent transcription 1, with nuclear localization and demonstrated genome-wide occupancy at target genes 2. Mechanistically, ZNF292 controls distinct developmental processes depending on cellular context. In cortical progenitors, it restrains differentiation by suppressing genes involved in neuronal differentiation and synapse formation 2. In differentiated interneurons, ZNF292 activates genes promoting maturation and function, including other neurodevelopmental disorder (NDD) genes 2. ZNF292 deficiency causes precocious progenitor differentiation followed by compromised interneuron maturation, altered channel activities, and neuronal hyperactivity 2. Pathogenic variants in ZNF292—predominantly de novo mutations—cause intellectual developmental disorder, autosomal dominant 64 (IDEV64), characterized by intellectual disability and autism spectrum disorder 1. ZNF292 emerges as a recurrent cause of neurodevelopmental disorders, identified in multiple large cohort studies 34. Beyond neurodevelopment, ZNF292 functions as a candidate tumor suppressor, harboring frameshift mutations in microsatellite-unstable gastric and colorectal cancers 5, and showing deletions in prostate cancer 6. Clinically, patients with ZNF292 variants typically present with mild to moderate intellectual disability with or without syndromic features including autism, developmental delay, and corpus callosum abnormalities 17.