ERK has been recognized as an important therapeutic target for glioblastoma.29 Sorafenib, the oral multikinase inhibitor approved for the treatment of hepatocellular carcinoma, modulates ERK dephosphorylation by targeting Raf.65, 66 Sorafenib‐inhibited NF‐κB activation was associated with ERK dephosphorylation,67 whereas limited activity was found in the combination of sorafenib and TMZ in patients with relapsed glioblastoma.25, 68 In our Western and IHC data, we provided evidence that imipramine significantly restrained the protein level of p‐ERK in glioblastoma (Figures 6C,D and 8B,E). Here, NFKB1 is linked to hepatocellular carcinoma.