To overcome this issue, we devised a strategy based on the dependence receptor properties of ALK, implying that in the absence of ligand or kinase activation, ALK is proapoptotic.21, 22 Using synthetic peptides to mimic the ALK proapoptotic domain (ADD),22 we showed human ALCL and neuroblastoma tumor cells were killed in a dose-dependent manner following incubation with an ADD-like peptide (P36). The gene discussed is ALK; the disease is neoplasm.