The identification of ALK-activating mutations in a subset of neuroblastoma tumors, the extremely low mutation rate of TP53 and the insufficiency of single-agent ALK or MDM2 inhibitors to inhibit the growth of this type of tumors prompted us to hypothesize that inhibition of the ALK pathway with concurrent induction of the p53 pathway might result in synergistic antitumor effects. Here, MDM2 is linked to neuroblastoma.