Abstract Background: High-risk neuroblastoma (NBL), driven by MYCN amplification, remains fatal for many children. Our previous work demonstrated that pharmacologic PP2A reactivation decreases NBL in vivo tumor growth through suppression of MYCN expression and stability by reducing MYCN phosphorylation and promoter acetylation, concurrent with BRD4 and RNA Pol II dephosphorylation. The current study is an extension of this previous work, in that we performed loss-of function tests validating the