To elucidate the mechanism by which Pon1 depletion impacts Phf8 and its downstream effects on mTOR, autophagy, and APP, we first examined whether the findings in Pon1−/− mice can be recapitulated in cultured mouse neuroblastoma N2a-APPswe cells that overproduce Aβ from a mutated human APP transgene [38]. The gene discussed is PHF8; the disease is neuroblastoma.