Most importantly,we provide a mechanistic perspective about the role of H19 in glioblastoma cells,by showing that its expression is inversely linked to that of NKD1,a negative regulator of Wnt pathway, suggesting that H19 might regulate NKD1 transcription via EZH2-induced H3K27 trimethylation of its promoter.Indeed, we showed that H19 binds EZH2 in glioblastoma cells,and that EZH2 binding to NKD1 and other promoters is impaired by H19 silencing.The molecular mechanisms described so far for an oncogenic role of H19 in GBM range from H19 processing to produce miR-675 to a function as sponge for miR-29a, in turn boosting tumor angiogenesis.