(39) and cell type specification (40–42). More recently, the model in which a transcription factor recruits complexes has been questioned by genomic studies in ES cells (11). Also, the ability of oncogenic BAF complexes to activate genes in heterochromatin where there is no detectable transcription factor binding strongly indicates that transcription factors are not necessary for recruitment of these complexes (see “BAF Complexes as Oncogenes: The SS18-SSX Fusion in Synovial Sarcoma”) (36). Finally, and most compellingly, recent exome sequencing studies conducted on a number of human diseases have shown that the subunits most commonly mutated in human disease were not those required for in vitro chromatin remodeling (4, 43–45).
