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In <i>Arabidopsis</i>, the salt overly sensitive (SOS) pathway, consisting of calcineurin B-like protein 4 (CBL4/SOS3), CBL-interacting protein kinase 24 (CIPK24/SOS2) and SOS1, has been well defined as a crucial mechanism to control cellular ion homoeostasis by extruding Na⁺ to the extracellular space, thus conferring salt tolerance in plants. CBL10 also plays a critical role in salt tolerance possibly by the activation of Na⁺ compartmentation into the vacuole. However, the functional relationship of the SOS and CBL10-regulated processes remains unclear. Here, we analyzed the genetic interaction between CBL4 and CBL10 and found that the <i>cbl4 cbl10</i> double mutant was dramatically more sensitive to salt as compared to the <i>cbl4</i> and <i>cbl10</i> single mutants, suggesting that CBL4 and CBL10 each directs a different salt-tolerance pathway. Furthermore, the <i>cbl4 cbl10</i> and <i>cipk24 cbl10</i> double mutants were more sensitive than the <i>cipk24</i> single mutant, suggesting that CBL10 directs a process involving CIPK24 and other partners different from the SOS pathway. Although the <i>cbl4 cbl10, cipk24 cbl10,</i> and <i>sos1 cbl10</i> double mutants showed comparable salt-sensitive phenotype to <i>sos1</i> at the whole plant level, they all accumulated much lower Na⁺ as compared to <i>sos1</i> under high salt conditions, suggesting that CBL10 regulates additional unknown transport processes that play distinct roles from the SOS1 in Na⁺ homeostasis.