For a short time, treatment in SH-SY5Y neuroblastoma cells, autophagy induction by 50 μM OLP results in an intermittent release of calcium (Ca2+) from the ER to activate the Ca2+/calmodulin-dependent protein kinase kinase-beta (CAMMKβ) which then phosphorylates AMP-activated protein kinase (AMPK).20 The same concentration of OLP used in N2a cells, for 3–48 h, decreases the phosphorylation of the mammalian target of rapamycin (mTOR) substrate, p70S6K. The gene discussed is MTOR; the disease is neuroblastoma.