A key mechanism by which plants adapt to salt stress involves maintaining ion homeostasis through ion transporters. This study identifies a role for the chloride channel (CLC) gene AtCLCf in salt tolerance in Arabidopsis thaliana. Under salt stress, AtCLCf is regulated by the WRKY transcription factor WRKY9 and translocates from the Golgi apparatus to the plasma membrane (PM), facilitating chloride ion (Cl⁻) efflux from roots and enhancing salt tolerance. Loss-of-function atclcf seedlings show increased sensitivity to salt, while overexpression of AtCLCf confers enhanced resistance. Salt stress induces the translocation of the GFP-AtCLCf fusion protein to the PM, and blocking this translocation with the exocytosis inhibitor brefeldin-A or mutating the small GTPase gene AtRABA1b/BEX5 increases salt sensitivity. Electrophysiology and liposome-based assays confirm that AtCLCf functions as a Cl⁻/H⁺ antiporter, facilitating Cl⁻ efflux from cells. The translocation of AtCLCf to the PM is mediated by the AtRABA1b/BEX5 pathway, which is essential for salt tolerance. AtCLCf is involved in Cl⁻ efflux and plays a critical role in maintaining Cl⁻ homeostasis in roots under salt stress. The study reveals that the translocation of AtCLCf from the Golgi to the PM under salt stress is a key mechanism for plant adaptation to salinity. This mechanism helps to remove excess Cl⁻ from roots, reducing its toxicity and increasing plant salinity tolerance. The findings highlight the importance of chloride channels in plant salt tolerance and provide insights into the molecular mechanisms underlying salt stress adaptation in plants.A key mechanism by which plants adapt to salt stress involves maintaining ion homeostasis through ion transporters. This study identifies a role for the chloride channel (CLC) gene AtCLCf in salt tolerance in Arabidopsis thaliana. Under salt stress, AtCLCf is regulated by the WRKY transcription factor WRKY9 and translocates from the Golgi apparatus to the plasma membrane (PM), facilitating chloride ion (Cl⁻) efflux from roots and enhancing salt tolerance. Loss-of-function atclcf seedlings show increased sensitivity to salt, while overexpression of AtCLCf confers enhanced resistance. Salt stress induces the translocation of the GFP-AtCLCf fusion protein to the PM, and blocking this translocation with the exocytosis inhibitor brefeldin-A or mutating the small GTPase gene AtRABA1b/BEX5 increases salt sensitivity. Electrophysiology and liposome-based assays confirm that AtCLCf functions as a Cl⁻/H⁺ antiporter, facilitating Cl⁻ efflux from cells. The translocation of AtCLCf to the PM is mediated by the AtRABA1b/BEX5 pathway, which is essential for salt tolerance. AtCLCf is involved in Cl⁻ efflux and plays a critical role in maintaining Cl⁻ homeostasis in roots under salt stress. The study reveals that the translocation of AtCLCf from the Golgi to the PM under salt stress is a key mechanism for plant adaptation to salinity. This mechanism helps to remove excess Cl⁻ from roots, reducing its toxicity and increasing plant salinity tolerance. The findings highlight the importance of chloride channels in plant salt tolerance and provide insights into the molecular mechanisms underlying salt stress adaptation in plants.