Furthermore, in accordance with the notion that a sustained and unrestrained activation of autophagy could support its functional switch from cytoprotection to cytotoxicity (see paragraph “Autophagic switch”), the combined treatment of ALK-mutated NB with Crizotinib and a strong inducer of autophagy (Rapamycin) was reported to enhance tumor cell death and to be beneficial for patients [120]. The gene discussed is ALK; the disease is neoplasm.