All in all, this study verified that AKR1B10 was notably downregulated, while ITGA5 was markedly upregulated in GC, and AKR1B10 hampered GC cell viability, invasion, migration, and adhesion by regulating ITGA5, through analysis of TCGA data along with clinical data, as well as in vitro molecular and cell experiments. This evidence concerns the gene ITGA5 and gastric cancer.