YK-4-279 and its clinical derivative TK-216 were developed in Ewing sarcoma based on their supposed ability to inhibit the interaction between EWSR1::FLI1 and an effector molecule RNA helicase A. In preclinical models, YK-4-279 functionally inhibited EWSR1::FLI1 activity, Ewing sarcoma cell and xenograft growth and caused G2/M arrest and apoptosis [22]. This evidence concerns the gene FLI1 and Ewing sarcoma.