Once JMJD3 expression was resumed from STAT3 inhibition, JMJD3 reduced the formation of neurosphere and cell proliferation of GSC.126 One of the treatment strategies for glioblastoma is an aptamer which targets the ligand of platelet-derived growth factor receptor A (PDGFRα), leading to decreased STAT3 and increased JMJD3 expression, and subsequent upregulation of p53.127 Collectively, these results suggested the central position of JMJD3 in the STAT3-JMJD3-p53 signal network that regulates glioma progression.128. This evidence concerns the gene KDM6B and glioblastoma.