RAG1 and acute myeloid leukemia: 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.