Although several studies focused on manipulating downstream pathways effected by the oncogenic fusion protein PAX3-FOXO1,32 ongoing clinical trials demonstrate that these treatments are not as effective as originally hoped.33, 34 Further, although inhibiting downstream pathways is logical, these treatments do not target the defining genetic aberration, PAX3-FOXO1, which was shown to directly contribute to many ARMS tumor phenotypes.35 Therefore, directly targeting PAX3-FOXO1 is logical for the development of novel pharmaceutical therapies to treat ARMS. Here, FOXO1 is linked to neoplasm.