Limited access to primary tumor makes it challenging to ascertain the status of molecular markers such as point mutations in ALK. While the most common ALK variants (R1275Q and F1174L) in neuroblastoma confer differential sensitivity to the kinase inhibitor crizotinib (39), a compound with promising results in a recent Phase I trial (31), identifying candidate patients for this targeted therapy and determining their mutation status is often impossible when primary tumor tissue is unavailable. This evidence concerns the gene ALK and neuroblastoma.