RAE1 mRNA and protein levels decrease upon inhibition of neuroblastoma cell proliferation, and its overexpression prevents retinoic acid-induced cell cycle arrest and differentiation [54]; however, a previous study demonstrated that RAE1/NUP98 mutant mice are more susceptible to DMBA-induced lung tumors compared to wild-type mice, indicating that combined RAE1/NUP98 haplo-insufficiency potentially promotes tumorigenesis [55]. This evidence concerns the gene NUP98 and neuroblastoma.