This notion is supported by our current work revealing downregulation of ATF5 in PRMT1 knockdown cells regardless of MYCN amplification status, and similar sensitivity in MYCN-non-amplified neuroblastoma cells to PRMT1 inhibition as that in MYCN-amplified cells, as well as by initial studies of ATF5 in neuroblastoma11. Here, MYCN is linked to neuroblastoma.