Unlike in lung carcinomas where the sensitivity and specificity of ALK IHC can be compared against ALK rearrangement status (as evaluated by FISH or CISH), such a ‘gold standard’ reference does not exist in neuroblastomas, since the mechanism for ALK protein expression does not appear to involve a genetic event in the majority of cases (as noted previously, the prevalence of strong ALK protein expression is generally 50% or higher, whereas the prevalence of ALK genomic amplification and/or mutations is around 10%). Here, ALK is linked to neuroblastoma.