AKT1 and cancer: NF-κB/p65 has always been documented as a key nuclear transcription factor against stimulation and stress and has been recognized as a downstreaming mediator of GRP78, PI3K/Akt, and ERK1/2 in cancer cells; the computational simulation noted the GRP78-NF-κB-binding interaction working as a potential neuroprotective pathway in brain injury [26, 29].