Additional cohorts of cells and mice bearing wild-type p53 would be necessary to determine whether the synergy between EWS-FLI1 and Stag2 occurs in wild-type p53 cells and whether the individual contributory roles of Stag2 loss and EWS-FLI1 to tumor formation as well as chromosomal aberrations, migration, invasion, and growth in soft agar. This evidence concerns the gene TP53 and neoplasm.