This differs from the significant enrichment of AP‐1 at IRF2BP2 binding sites observed in AML and neuroblastoma.[44, 45] We propose that in T‐ALL, IRF2BP2 collaborates with master TFs to regulate the expression of the critical susceptibility gene RAG1, reshaping the intracellular environment and driving its oncogenic potency. This evidence concerns the gene RAG1 and neuroblastoma.