For example, a heterozygous deletion of p53 in Th-MYCN mice has increased tumorigenesis and resistance to the anti-tumor drug cyclophosphamide.13 Similarly, mutant ALK (ALKF1174L and ALKR1279Q) has significantly promoted tumorigenesis in Th-MYCN mice,14,15 while the deletion of caspase-8 has substantially heightened the metastatic potential of neuroblastoma into the bone marrow.16 Conversely, midkine knockout in Th-MYCN mice has inhibited neuroblastoma growth.17 Despite these insights, spontaneous regression of neuroblastoma has not been modeled so far owing to its enigmatic mechanisms. The gene discussed is ALK; the disease is neuroblastoma.