NAB2 (NGFI-A binding protein 2) functions as a transcriptional corepressor that regulates zinc finger transcription factors and controls gene expression through multiple mechanisms. In normal cellular contexts, NAB2 acts as a negative regulator of transcription, with specific isoforms exhibiting differential repression capacity. Clinically, NAB2 is most significant in its pathogenic role through fusion with STAT6. The NAB2-STAT6 fusion is the defining molecular alteration of solitary fibrous tumors (SFTs), a soft tissue sarcoma 12345. This fusion event leads to nuclear relocalization of STAT6 protein, detectable by immunohistochemistry, with exon 4-STAT6 exon 3 fusions correlating with classic SFT morphology and potentially less aggressive behavior 5. NAB2-STAT6 fusions have been identified in meningeal and non-meningeal SFTs as well as hemangiopericytomas, unifying these previously distinct entities into a single disease continuum 45. Importantly, NAB2-STAT6 fusion status is used for risk stratification in SFTs to predict metastatic potential 1. Beyond neoplasia, NAB2 regulates intramuscular adipogenesis by driving CFD expression in fibro-adipogenic progenitors, with elevated CFD-NAB2 signaling observed in human metabolic syndrome and Duchenne muscular dystrophy, correlating with pathological fat accumulation 6.