In glioma, IKBKE promoted the translocation of NF‐κB transcription factors composed of a heterodimer of p50 and p65 subunits into the nucleus and initiated the transcription of downstream factors of the NF‐κB signaling pathway to accelerate the progression of glioma.30, 31 Zhang et al33 pointed out that PLK4 could directly phosphorylate IKBKE at Ser‐36 to sensitize it, thus activating the NF‐κB pathway to enhance glioblastoma chemotherapy resistance. This evidence concerns the gene NFKB1 and central nervous system cancer.