Around 8–10% of sporadic NB tumours present with point mutations in the kinase domain of the full-length ALK receptor [22,23]; this is in contrast to the oncogenic NPM-ALK and EML4-ALK fusions that drive ALK-positive anaplastic large cell lymphoma (ALCL) and non-small cell lung cancer (NSCLC), respectively. This evidence concerns the gene EML4 and non-small cell lung carcinoma.