Artificially silencing the expression of H2AFJ predominantly repressed the mRNA levels of TNF-alpha and interleukin-6 in D54MG glioblastoma cells (Figure 4H), whereas the forced gene expression of ectopic H2AFJ dramatically enhanced the expression of TNF-alpha and interleukin-6 in T98G glioblastoma cells (Figure 4I). Here, IL6 is linked to glioblastoma.