The salt overly sensitive (SOS) pathway is the only mechanism known for Na extrusion in plant cells. SOS pathway activation involves Ca-sensing proteins, such as calcineurin B-like (CBL) proteins, and CBL-interacting protein kinases (CIPKs). In this signalling mechanism, a transit increase in cytosolic Ca concentration triggered by Na accumulation is perceived by CBL (also known as SOS3). Afterward, SOS3 physically interacts with a CIPK (also known as SOS2), forming the SOS2/SOS3 complex, which can regulate the number downstream targets, controlling ionic homeostasis. For instance, the SOS2/SOS3 complex phosphorylates and activates the SOS1 plasmalemma protein, which is a Na/H antiporter that extrudes Na out of the cell. The CBL-CIPK networking system displays specificity, complexity and diversity, constituting a critical response against salt stress and other abiotic stresses. In a study reported in the journal Plant and Cell Physiology, we showed that NH induces the robust activation of transporters for Na homeostasis in root cells, especially the SOS1 antiporter and plasma membrane H-ATPase, differently than does NO. Despite some studies having shown that external NH ameliorates salt-induced effects on ionic homeostasis, there is no evidence that NH per se or some product of its assimilation is responsible for these responses. Here, we speculate about the signalling role behind glutamine in CBL-CIPK modulation, which could effectively activate the SOS pathway in NH-fed stressed plants.