Given the sufficiency of SIX1 KD to promote EWS/FLI1-low-like phenotypes in this context, and the observation that EWS/FLI1 stabilizes SIX1 protein levels, it begs the question as of whether SIX1 is a critical downstream effector of many EWS/FLI1-driven phenotypes in ES. This evidence concerns the gene FLI1 and Ewing sarcoma.