LNG exhibited a potent hepatoprotective activity and an effective neuroprotective potential that significantly hampered the progression of HE following TAA administration by modulating various inflammatory mediators: COX‐2, IL‐1β, and TNF‐α, together with the transcription factor, CCAAT/enhancer binding protein beta (C/EBPbeta), and the chemokine, CX3CL1, which modify microglial activation during neuroinflammation in acute HE [106]. This evidence concerns the gene CEBPB and hereditary elliptocytosis.