Although the molecular reasons that sarcomas prefer the usage of RBPs as their drivers remain unknown, EWS/FLI1, for example, recruits the SWI/SNF complex to directly establish super-enhancers on the loci different from the binding sites of wildtype EWS (this process is mainly achieved by the TAD of EWS), which is also supported by LAD-mediated phase separation. This evidence concerns the gene SMARCA1 and sarcoma.