We know from previous work that ALK activation drives transcription of MYCN and potentiates MYCN‐driven NB in mouse and zebrafish models (Weiss et al, 1997; Berry et al, 2012; Heukamp et al, 2012; Schonherr et al, 2012; Zhu et al, 2012; Cazes et al, 2014; Ono et al, 2019), and this is supported by analysis of NB tumours where coexistence of ALK activating mutations and MYCN amplification forms a high‐risk NB group with poor prognosis (De Brouwer et al, 2010). This evidence concerns the gene ALK and neoplasm.