Gastric carcinoma remains one of the most prevalent forms of cancer worldwide, 
despite the decline in incidence rates, increased awareness of the disease and 
advancement in treatment strategies. Helicobacter pylori infection, dietary 
factors, lifestyle influences and various genetic aberrations have been shown to 
contribute to the development and progression of gastric cancer. Recent studies 
on the genomic landscape of gastric adenocarcinoma have identified several key 
signaling molecules, including epidermal growth factor receptor family (ErbB) 
members, vascular endothelial growth factor receptor family (VEGFR) members and 
PI3K/Akt/mTOR pathway components, that have been implicated in the molecular 
pathogenesis of gastric cancers. However, clinical trials with compounds that 
target these molecules have failed to show a significant improvement in overall 
survival rates when supplemented with conventional therapies. Therefore, it is 
essential to identify effective prognostic and/or diagnostic biomarkers and 
develop molecular targeted therapies. The JAK/STAT cascade is a principal signal 
transduction pathway in cytokine and growth factor signaling, regulating various 
cellular processes such as cell proliferation, differentiation, migration and 
survival. Numerous in vivo and in vitro studies have shown that dysregulated 
JAK/STAT signaling is a driving force in the pathogenesis of various solid 
cancers as well as hematopoietic malignancies. Hence, a large number of 
preclinical and clinical studies of drugs targeting this pathway are currently 
underway. Notably, aberrant JAK/STAT signaling has also been implicated in 
gastric cancers. In this review, we focus on the ongoing research on the 
JAK/STAT cascade in gastric carcinoma and discuss the therapeutic potential of 
targeting JAK/STAT signaling for the treatment of gastric cancer.