The discovery of the extensive role of ATP-dependent chromatin remodeling in cancer has highlighted several important goals for the future. The precise mechanism of tumor suppression used by these complexes must be understood if therapeutic advances are to be made. This fundamental mechanism is characterized by dosage sensitivity, tumor specificity, and the fact that this mechanism cannot be detected using present in vitro assays. These mechanisms are likely to be shared with those used in neural development. Hence, a major goal for the future is to develop new assays that faithfully predict the oncogenic functions of the complexes. The discovery that BAF complexes can also be oncogenes and definitive drivers of cancer has led to the realization of a true cancer-specific avenue toward therapeutic development for synovial sarcoma. The biochemical pathways that are likely to modulate BAF complex function must be understood as potential susceptibility factors for cancer. Finally, the possibility of inhibition of homologous subunits may prove a fruitful approach.
