In summary, dynamic expression profiling following ALK inhibition of ALK mutated neuroblastoma cells revealed (1) unexpected early ADM upregulation with potential implications for design of more effective ALK targeted therapy, (2) an initial increase of MYC(N) activity immediately after ALK inhibition and (3) confirmed inhibition after 1 to 2 hours of the ALK downstream MAPK, PI3K-AKT, RET and MYC(N) pathways. The gene discussed is AKT1; the disease is neuroblastoma.