Another study reported that within the NF-κB-RNF2-KLF9 cascade, KLF9 serves as a key downstream effector mediating GPR17’s antiproliferative and pro-apoptotic roles in glioma pathogenesis, offering a dual targeting strategy involving GPR17 activation or KLF9 modulation (88). This evidence concerns the gene GPR17 and central nervous system cancer.