These results combined with the well-established association between up-regulated expression of miR483 and tumorigenesis11,12,16–18 implies that disruption of the ZBED6-Igf2 axis, either by impairing ZBED6 expression or blocking its access to the binding site in an intron of Igf2, can promote tumor growth in those cell types where ZBED6 suppresses miR483 expression. Here, IGF2 is linked to neoplasm.