In NB, the constitutively activated ALK is complexed with hyperphosphorylated ShcC,15 deregulating the MAPK pathway response to growth factors.16 Another relevant genetic feature in neuroblastoma is the loss-of-function mutations or deletions of the RNA-helicase ATRX.17, 18 In a study of 240 NB cases using a combination of whole-exome, genome and transcriptome sequencing Pugh et al.19 observed putative loss-of-function ATRX alterations in 9.6% of cases (6 mutations and 17 multi-exon deletions). The gene discussed is SHC3; the disease is neuroblastoma.