In order to investigate the clinical relevance of our observations that both NF1 loss and NRAS activation were sufficient to induce ALK inhibitor resistance in neuroblastoma models, we genomically profiled tumor and liquid biopsy samples (whole-exome sequencing or a hybrid-capture targeted next-generation sequencing assay) from four patients with neuroblastomas harboring activating ALK mutations before ALK inhibitor treatment and during tumor progression under treatment (Fig. 5a, also see Table S1). The gene discussed is ALK; the disease is neuroblastoma.