Recently, the molecular pathogenesis of AFH has become clarified by the discovery of fusion genes resulting from various chromosomal translocations, including the most prevalent EWSR1-CREB1 derived from t(2;22)(q33;q12),16 followed by EWSR1-ATF1 from t(12;22)(q13;q12),17 and the least common FUS-ATF1 from t(12;16)(q13;p11).18 Thway et al expanded the clinicopathological spectrum of AFH by characterizing 13 AFH cases by fluorescence in situ hybridization (FISH) and reverse transcription polymerase chain reaction (RT-PCR). The gene discussed is CREB1; the disease is histiocytoma, Angiomatoid fibrous.