THAP2 is a nuclear protein containing a THAP domain that functions as a regulatory target in cellular stress responses and cancer progression. Mechanistically, THAP2 expression is negatively regulated by microRNAs, including miR-100 and miR-99b-5p 12. In prostate cancer, THAP2 is significantly downregulated in metastatic disease compared to localized high-grade carcinoma, suggesting its involvement in controlling cancer progression 3. THAP2 suppression appears context-dependent: in endothelial cells exposed to high glucose stress, THAP2 inhibition by miR-99b-5p-carrying exosomes promotes cell growth, migration, and angiogenic capacity 2, while in prostate cancer, reduced THAP2 levels associate with metastatic transformation 3. The miR-100-mediated downregulation of THAP2 occurs at both mRNA (38% reduction) and protein levels (34-69% reduction) in prostate cancer cell lines 1. These findings indicate THAP2 functions as a context-dependent regulator where its suppression promotes protective angiogenic responses in metabolic stress but may facilitate oncogenic progression in cancer. Further investigation is needed to elucidate THAP2's intrinsic molecular functions and transcriptional roles in these distinct pathological contexts.