Thus, more neuroblastoma-optimized therapy approaches aiming at oncogenic molecular targets, for example, affecting neuroblastoma cell maturation and proliferation, are believed to improve therapeutic efficacy, reduce toxicity and avoid long-term side effects.2 Small molecules, which influence gene transcription, for example, histone deacetylase (HDAC) inhibitors, are known to induce maturation of differentiation-defective tumor cells, such as neuroblastoma cells (reviewed in Witt et al.3). Here, HDAC9 is linked to neuroblastoma.