FLI1 and Ewing sarcoma: We suspect that this widespread disruption of EWS-FLI1 activity may be responsible for the heightened sensitivity of Ewing sarcoma cells to actinomycin D. These results are reminiscent of prior studies demonstrating that mithramycin and ET-743 (trabectedin), both DNA binding agents, reduced expression of EWS-FLI1 downstream targets and inhibited the growth of Ewing sarcoma cells [11], [12].