Because SIX1 has the opposite effect on ES metastasis than it does in all previously studied tumor types11,13–16,18,28–30, we hypothesized that this anti-metastatic effect may be due to the concomitant expression of the transgene EWS/FLI1, which regulates many phenotypes in a similar manner to what we have observed with SIX1, including promoting anchorage-independent growth (Fig. 1i–l) while repressing metastatic features (Fig. 2a–h)6,7. Here, FLI1 is linked to neoplasm.