Among the different proposed mechanisms for NGB antiapoptotic role, the direct involvement of NGB in the intrinsic apoptotic pathway at mitochondrial level has been identified in neurons.13 As reported here, also in non-nervous cancer cells, as well as in neuroblastoma cells, E2 treatment significantly increases the amount of NGB in the mitochondrial compartment, strengthening the idea that NGB could represent the intracellular mediator of the E2 antiapoptotic effect in ERα-encoding cancer cells, acting directly in the mitochondria, where the core of the intrinsic apoptotic pathway initiates. The gene discussed is ESR1; the disease is neuroblastoma.