Due to space limitations and for clarity and simplicity, only the sequence portion of the NF-κB binding site mutation (M2) and STAT3 binding site mutation were presented for the double mutant in Supplementary Fig. 3A. Subsequently, we transfected glioma cell lines A172, U87MG, and PDX-L14 with constructs containing FOSL1 wild type promoter (FOSL1 luc), as well as variants harboring mutations in the NF-κB combined binding site (M1-5), mutations in the STAT3 binding site (STAT3 mut), and the double mutant. The gene discussed is FOSL1; the disease is central nervous system cancer.