The predictable emergence of resistance to tyrosine kinase inhibitors (TKIs), leading to disease progression or relapse, has hindered their long-term therapeutic impact.1 This obstacle is best exemplified by the development of resistance to imatinib in BCR-ABL-expressing chronic myeloid leukemia and gefitinib in EGFR-mutant non-small-cell lung cancer,2, 3 and is likely to impede efforts to devise effective targeted therapy for many other cancers, including neuroblastoma (NB). This evidence concerns the gene ABL1 and neuroblastoma.