ATM and neuroblastoma: To understand whether the cerebellar dysregulations of old ATM-null mice are due to ATM absence as a platform for protein complex formation, or absent ATM kinase activity, we assessed if they are recapitulated after stress in neuroblastoma cells upon KD of ATM mRNA, or after treatment with KU-55933 (KU) as a pharmacological inhibitor of ATM-mediated phosphorylation (scheme and control of ATM mRNA levels in Figure 4a,b).