However, it is clear that spontaneously active TrkAIII acts in a manner analogous to neurotrophin-activated cell surface TrkA in its capacity to reorganise and promote MT assembly in vivo but does so at the centrosome rather than cell periphery, resulting in the promotion and maintenance of a proliferating, undifferentiated NB cell phenotype rather than inducing neuronal differentiation, which results from cell surface TrkA activation (this study [1, 8–10]). The gene discussed is BDNF; the disease is neuroblastoma.