THAP7 (THAP domain containing 7) is a chr22-associated transcriptional repressor that functions as a dual-activity protein integrating histone modifications with gene silencing. As a primary function, THAP7 binds preferentially to hypoacetylated histone H4 tails via its C-terminal 77 amino acids and recruits histone deacetylase 3 (HDAC3) and nuclear hormone receptor corepressor (NCoR) to promoters, promoting histone H3 hypoacetylation and transcriptional repression 1. THAP7 also associates with template-activating factor-Ibeta (TAF-Ibeta), another corepressor that maintains histones in a hypoacetylated state 2. Mechanistically, THAP7's conserved THAP domain is critical for HDAC3 association, while both the THAP domain and histone-interaction domain are essential for full repressive activity 1. Beyond its canonical transcriptional role, THAP7-AS1, a long noncoding RNA transcribed from the THAP7 locus, has emerged as an oncogenic factor in multiple cancers. In gastric and lung cancer, THAP7-AS1 is upregulated and stabilized via METTL3-mediated m6A modification, promoting cancer cell proliferation and invasion through CUL4B-dependent repression of tumor-suppressive microRNAs and PI3K/AKT pathway activation 34. In ischemic stroke, THAP7-AS1 interacts with EIF3A to enhance ITPR1 expression, promoting endothelial cell pyroptosis and ER stress 5. Genome-wide association studies have identified THAP7 variants associated with diabetic kidney disease susceptibility 6. These findings position THAP7 as both a fundamental chr22 regulator and an emerging therapeutic target in cancer and vascular disease.