HSPA5 and neuroblastoma: The result is chronic oncogenic signaling through IP3K/Akt but not Ras/MAPK, a pro-survival ER-stress response characterised by ATF6 activation and increased Grp78/Bip expression, a more angiogenic and stem cell-like phenotype, centrosome amplification and genetic instability, increased resistance to ROS and chemotherapeutic agent-induced death and enhanced primary and metastatic tumour growth in NB models [1, 2, 6–12].