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). The gene discussed is TF; the disease is acute lymphoblastic leukemia.