GTF2I (general transcription factor IIi) is a ubiquitously expressed transcription factor that coordinates formation of multiprotein complexes at gene promoters, particularly the C-FOS serum response element, and links signal-responsive activator complexes to basal transcription machinery 1. It functions as a coregulator for multiple transcription factors including USF1 and ARID3A, promoting RNA polymerase II-dependent transcription 1. GTF2I plays critical roles in neurodevelopment and hematopoiesis. In cortical development, GTF2I regulates neural progenitor proliferation and neuronal differentiation in a dosage-dependent manner; duplication causes excessive excitatory neuron production linked to autism-spectrum disorder through the GTF2I-LSD1 axis 2. Loss of GTF2I increases neural progenitor proliferation but impairs synaptic development, increasing neuronal apoptosis and reducing electrophysiological activity 3. In erythroid cells, GTF2I acts as a repressor of adult β-globin transcription while positively regulating fetal γ-globin and stress response genes including ATF3 and CHOP 4. Clinically, GTF2I is a key mediator of cognitive and behavioral phenotypes in Williams syndrome (caused by 7q11.23 microdeletion) and 7q11.23 microduplication syndrome 12. GTF2I is also implicated in inflammatory bowel disease susceptibility and has been identified in acute promyelocytic leukemia translocation variants 56. Additionally, GTF2I phosphorylation at S784 by ERK mediates ALDH1A1 upregulation in response to KRAS inhibitors 7.