A673 cells harbor a BRAFV600E mutation and are also known to have constitutive activation of PI3K27, and it has previously been shown that even KD of EWS/FLI1, the main driver of ES oncogenesis, does not inhibit the growth of A673 cells in adherent conditions, but does suppress anchorage-independent growth7. Here, FLI1 is linked to Ewing sarcoma.