In high-risk neuroblastoma, identification of ALK activating genetic alterations is considered for clinical decision-making in a relapse setting or more recently in frontline treatment. The accurate diagnosis of genetic alterations requires harmonization of molecular techniques and reporting, especially when these are considered as inclusion criteria for clinical trials. Analysis and validation were performed across the 21 SIOPEN (International Society of Paediatric Oncology Europe Neuroblastoma) molecular diagnostic laboratories, with 14 DNA samples harboring distinct ALK alterations. These included ALK mutations at or outside hotspots in the tyrosine kinase domain with variant allele frequencies (VAFs) ranging from 1% to 91% or ALK genomic amplification shared between the laboratories. Each laboratory used their own established techniques: ALK amplifications were detected by using either pan-genomic copy number techniques or fluorescence in situ hybridization, and ALK mutations were characterized by next-generation sequencing techniques. All laboratories correctly identified high-level ALK amplification and ALK mutations within the tyrosine kinase domain hotspots with VAF >5%, with the exception of two cases. Differences in interpretation and reporting were apparent for samples harboring mutations with a VAF