From this perspective, CHK1 inhibitors capable of activating caspase-2 may be beneficial, at least in part, for non-MYCN amplified neuroblastomas bearing a deficiency in DNA repair pathways, such as neuroblastomas with 11q loss, since loss of caspase-2 delayed tumorigenesis in TH-MYCN mice but accelerated it in Atm-/-caspase-2-/-mice, as described above. This evidence concerns the gene ATM and neuroblastoma.