INTS7 is a core component of the integrator complex, a multiprotein machine that regulates RNA polymerase II (Pol II) transcription termination in the promoter-proximal region of genes 12. The complex functions as a quality checkpoint during transcription elongation, terminating unfavorably configured transcripts through three coordinated mechanisms: dephosphorylation of Pol II's C-terminal domain, endonucleolytic degradation of nascent RNA, and release of Pol II from DNA 12. Beyond protein-coding genes, INTS7 participates in terminating non-coding Pol II transcripts including enhancer RNAs, snRNAs, and lncRNAs 3. The gene also contributes to DNA damage response signaling during S phase 4. Clinically, INTS7 variants associate with multiple disease conditions. Genome-wide association studies implicate INTS7 in schizophrenia and bipolar disorder susceptibility 5, asymptomatic intracranial large artery stenosis in multi-population cohorts 67, and cannabis use susceptibility 8. In lung adenocarcinoma, elevated INTS7 expression promotes tumor progression by suppressing immune infiltration and activating p38MAPK signaling 9. Pan-cancer analysis reveals INTS7 mutations and transcriptional alterations across multiple tumor types 10. These findings suggest INTS7 plays functionally diverse roles in transcriptional regulation, genome stability, and disease pathogenesis.