The broad range of ALK mutations found either as a secondary resistance mechanism to ALK inhibition in NSCLC or as a primary resistance mechanism in neuroblastoma necessitates thorough interrogation of the ability of individual compounds to inhibit ALK phosphorylation and subsequent survival signaling downstream of ALK, enabling the rapid translation of the most promising compounds from the laboratory to clinical trials (Bresler et al., 2011, 2014). This evidence concerns the gene ALK and neuroblastoma.