TCEAL1 encodes a nuclear phosphoprotein that functions as a transcriptional regulator, modulating gene expression in a promoter-dependent manner without directly binding DNA 1. The protein shares sequence homology with transcription elongation factor TFIIS and competes with TFIIS for binding to core promoters 2. TCEAL1 forms a complex with the deubiquitinating enzyme USP11, which protects TCEAL1 from proteasomal degradation while TCEAL1 recruits USP11 to RNA polymerase II 2. This complex promotes transcription elongation and maintains expression of essential genes, including RPB8, a subunit of all nuclear RNA polymerases 2. Loss-of-function variants in TCEAL1 cause Hijazi-Reis syndrome, an X-linked neurodevelopmental disorder characterized by intellectual disability, developmental delay (especially affecting expressive speech), autistic behaviors, hypotonia, and dysmorphic facial features 34. Additional features include gastrointestinal, ocular, and endocrine abnormalities, with adult patients showing hyperphagia, obesity, and metabolic dysfunction including type 2 diabetes 45. TCEAL1 suppression has been shown to enhance docetaxel efficacy in prostate cancer by altering cell cycle profiles and increasing apoptosis 6, suggesting potential therapeutic applications in oncology.