Respiratory burst oxidase homolog (Rboh) genes play a crucial role in stress tolerance by encoding NADPH-oxidase proteins responsible for H2O2 production. This study delves into the function of the tomato SlRbohG gene in salt stress tolerance through the characterization of two salinity-hypersensitive allelic mutants, sodium gatherer1 (sga1) and sga2. These mutants display prominent chlorosis and swelling when subjected to saline stress, which is associated with an increase in Na+ and water transport from roots to shoots. Accordingly, a significant decrease in the expression levels of crucial sodium transporter and aquaporin genes was detected in both mutants. By combining mapping-by-sequencing and CRISPR/Cas9 methods, we unveiled that mutations within the SlRbohG coding sequence are responsible for the sga phenotype. In wild-type (WT) plants, exposure to salt triggered an increased in H2O2 production in both shoots and roots, correlating with heightened SlRbohG expression. However, this salt-induced H2O2 raise was absent in sga mutants. WT plants treated with the NADPH oxidase inhibitor DPI halted H2O2 production in response to salinity, resulting in increased Na+ contents in shoots and decreased SlHKT1;2 expression levels in roots. In long-term salt treatment trials, sga mutants exhibited a significant accumulation of Na+ in their reproductive organs, leading to a drastic reduction in fruit production. Hence, our results not only highlight the SlRbohG role in ROS-mediated signaling but also emphasize its function in preventing the harmful accumulation of excessive Na+ in the aerial parts, thereby playing a crucial role in ensuring salt tolerance response of tomato plants.