Given the association ofMEG3 with a repressive chromatin modifier, EZH2, one would expect thatthe upregulated genes are more direct targets of the MEG3/EZH2 interaction.On the other hand, MEG3 peaks also flanked the genes that showed repressionin the absence of MEG3. We suggest that the expression of these genes may befacilitated by the recruitment of EZH2 by MEG3, and this EZH2-dependentactivation of genes was evident in recent findings where EZH2 has been shown to actas a coactivator of gene expression in prostate and breast cancer cells55, 56. This evidence concerns the gene MEG3 and breast carcinoma.