A large body of literature has demonstrated that the PI3K/AKT pathway plays an important role in TMZ resistance,14 and evidence exists that glioma is resistant to TMZ via the PI3K/AKT/NF‐κB signaling cascade.15 Especially, activation of NF‐κB is a general cellular response to anticancer drugs.16 Therefore, the treatment of TMZ is likely to also activate NF‐κB through some mechanisms. Here, NFKB1 is linked to central nervous system cancer.