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. This evidence concerns the gene CASP8 and neuroblastoma.