In stable transfected TrkAIII-expressing SH-SY5Y NB cells, intracellular cell cycle-regulated ligand-independent TrkAIII activation induces pro-survival PI3K/Akt signaling, enhances Bcl-xL, Mcl-1 and SOD2 expression, promotes a pro-angiogenic MMP-9/VEGF/Tsp1 expression equilibrium and a more anaplastic stem cell-like phenotype, induces centrosome amplification and modifies the endoplasmic reticulum (ER) stress response [6,7,19]. The gene discussed is AKT1; the disease is neuroblastoma.