While SIX1 complex inhibitors (targeting either SIX1 or its critical cofactor, EYA proteins) are currently in development for the treatment of other tumor types10,24,25, these findings suggest that targeting of SIX1 in ES may actually promote metastasis and tumor progression, and emphasize the importance of additional studies into the role of SIX1 in different sarcomas or fusion-driven tumors to determine the generalizability of these findings to similar tumor types. This evidence concerns the gene SIX1 and neoplasm.