In follow-up to our initial study, which established a 77-gene signature driven by constitutive ALK signalling5, we performed a time series analysis of ETV5 expression levels upon pharmacological ALK inhibition using the same ALK-specific tool compound (TAE-68416,17) in neuroblastoma cell lines carrying the ALK hotspot mutations ALKR1275Q (CLB-GA) and ALKF1174L (SH-SY5Y), ALK amplification (ALKamp, NB-1) and wild-type ALK (ALKwt,SK-N-AS, which harbours the NRASQ61K mutation). This evidence concerns the gene ALK and neuroblastoma.