In conclusion, CBN may inhibit the AKT pathway by affecting CBR2 expression, leading to a p53-dependent or -independent transactivation of miR-34a; the latter directly silences E2F1 and guides the production of tRiMetF31 which targets PFKFB3, eventually resulting in suppression of neuroblastoma proliferation, invasion, and angiogenesis (Figure 7), highlighting novel and crucial tumor suppressor miR-34a/tRiMetF31/PFKFB3 axis in CBN’s antineuroblastoma actions. Here, E2F1 is linked to neuroblastoma.