BRD4 and ependymoma: Similar mechanisms are observed in FET family (FUS, EWS, TAF15) fusions [151], BRD4-NUT fusions [152], and YAP fusions [153], which form oncogenic condensates that recruit ATP-dependent chromatin remodeling complexes BAFs (Brg/Brahma-associated factors), histone acetyltransferase p300, and Pol II to enhance chromatin accessibility and oncogene expression, driving malignancies such as sarcomas [154,155,156], midline carcinomas [157,158,159], and ependymomas [153].