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). Here, GLI1 is linked to acute lymphoblastic leukemia.