EWS-FLI1 uses divergent chromatin remodeling mechanisms to induce an open chromatin state of GGAA microsatellites, creating EwS-specific enhancers that physically interact with target gene promoters and/or enhancers, inducing oncogene activation and repressing tumor suppression (Riggi et al., 2014; Johnson et al., 2017). This evidence concerns the gene EWSR1 and neoplasm.