Mechanistically, TF dysregulation in pediatric tumors arises through chromosomal rearrangements (e.g., ETV6::RUNX1 in acute lymphoblastic leukemia (ALL), EWS::FLI1 in Ewing sarcoma), overexpression (MYCN in NB, GLI1 in Sonic Hedgehog (SHH) medulloblastoma (MB)), or mutations (PHOX2B, TP53, MYOD1 in spindle cell RMS). This evidence concerns the gene TF and neuroblastoma.