GLS and Hyperammonemia: Another recent study investigating TNF‐α in HE‐related neuroinflammation has revealed that both the tumor necrosis factor receptor 1 (TNFR1)‐CCL2‐BDNF‐tropomyosin receptor kinase B (TrkB)‐KCC2 and TNFR1‐NF‐kB‐glutaminase‐GAT3 pathways via elevated TNF‐α lead to increased GABAergic transmission by the Purkinje neurons and are associated with motor deficits induced by hyperammonemia [23], showing that microglia‐derived TNF‐α can drive the subsequent GABAergic signaling in the cerebellum.