While JMJD6 is associated with super-enhancers, treatment with THZ1 and the histone deacetylase (HDAC) inhibitor panobinostat synergistically reduced JMJD6, E2F2, N-Myc, and c-Myc expression, induced tumor cell apoptosis in vitro, and led to neuroblastoma tumor regression in mice, which were significantly reversed by forced JMJD6 overexpression, suggesting this combination as a therapeutic approach for neuroblastoma. The gene discussed is MYC; the disease is neoplasm.