Interestingly, overexpression of RHA increases Ewing sarcoma resistance to genotoxic stress, but not non-sarcoma cancer cells [89, 19], indicating that the underlying mechanism involves RHA/EWS-FLI1 interaction and confirming that the activity of RHA is dependent on its molecular partners [91, 19]. This evidence concerns the gene EWSR1 and Ewing sarcoma.