Background <p>Soil salinization severely limits sweet cherry (<i>Prunus avium</i> L.) growth and productivity, yet the NHX (Na⁺/H⁺ antiporter) gene family, which is central to salt tolerance, remains uncharacterized in this species.</p> Results <p>Through genome‑wide identification, we identified 37 <i>PavNHX</i> genes unevenly distributed on eight chromosomes. Subcellular localization predictions revealed 21 PavNHX proteins on the cell membrane and 16 in the vacuole. Phylogenetic analysis divided the family into three groups; Group I shared homologs with Arabidopsis, indicating evolutionary conservation. qRT‑PCR under salt stress showed that <i>PavNHX37</i> was the most strongly induced gene (8.9‑fold at 150 mM NaCl), and its Cell membrane localization was experimentally confirmed. Stable overexpression of <i>PavNHX37</i> in <i>Nicotiana benthamiana</i> significantly improved salt tolerance: transgenic lines exhibited lower Na⁺ accumulation, higher K⁺ retention, and a reduced Na⁺/K⁺ ratio, along with better growth, higher proline accumulation, elevated SOD, POD and CAT activities, and reduced MDA content under 150 mM NaCl compared to wild‑type plants.</p> Conclusion <p>This study provides the first systematic characterization of the NHX family in sweet cherry and demonstrates that <i>PavNHX37</i> enhances salt tolerance by maintaining Na⁺/K⁺ homeostasis and boosting antioxidant capacity, offering genetic resources for molecular breeding.</p>