TrkAIII exerts its “oncogenic” activity in NB cells by: protective IP3K/Akt/NF-κB signalling; induction of a pro-angiogenic pattern of gene expression; interacting with the centrosome, promoting centrosome amplification, peri-nuclear microtubule assembly and genetic instability; increasing the level of sister chromatid exchange; and modulating the unfolded protein response, pre-conditioning and adapting cells to stress [1]–[5]. This evidence concerns the gene ITPKB and neuroblastoma.