JAK1 and gastric adenocarcinoma: The phosphorylation of a critical tyrosine residue (Tyr705) triggers STAT3 dimerization by contacting the phosphotyrosine-SH2 domain, thus mediating activation of STAT3, which binds to DNA sequences to stimulate target genes. JAK1/STAT3 is upstream of IL-8 and NF-κB in Helicobacter-infected gastric epithelial cells [104], and p-STAT3 level is related to poor survival in gastric adenocarcinoma patients [142].