Early developmental studies in Drosophila foreshadowed the opposing, antagonistic functions of Trithorax (of which BAF is a member) and Polycomb complexes in the regulation of mammalian gene expression and, more recently, cancer. The antagonistic nature of BAF and Polycomb complexes has emerged as a likely culprit in causing extensive, misplaced repression (or in some cases, activation) genome-wide (Fig. 5). The clearest example of this came from studies by Roberts and colleagues, who discovered that BAF47-deficient MRTs displayed marked increases in the H3K27me3 repressive mark, a mark known to be placed only by PRC2 complexes. Given the important tumor-suppressive function of p16-INK4A, several groups honed in on this locus to reveal the extensive repression over this site in the setting of BAF47 (SNF5) loss (69, 109). From studies in ES cells, we know that BAF complexes oppose PRC complexes at most sites, with the exception of genes such as the Hox loci at which they appear to act synergistically to enable the placement of the H3K27Me3 mark (11). This is in marked contrast to Drosophila, where BAF opposes Polycomb at the
