This bears similarity to NGF-activated TrkA protection of sympathetic neuroblast against KIF1Bβ-dependent death [26, 27] and suggests that TrkAIII, which associates with NB, may facilitate NB initiation by preventing KIF1Bβ-induced death in a manner analogous to 1p36-deletion of KIF1B, germline KIF1B mutations or Nmyc amplification [25–32]. The gene discussed is NGF; the disease is neuroblastoma.