In gastric, colorectal, liver, and pancreatic cancer, most studies have found ANXA2 to be overexpressed, promoting oncogenesis by interacting with other molecules and signaling pathways; in GC, namely the p38MAPK and AKT pathways; in CRC, gastrin-like peptides, tenascin-C, LINC00460, as well as the Src/ANXA2/STAT3 pathway; in HCC integrins, CD147, UBAP2 and the RhoA/ROCK, Rac1/WAVE2 and integrin-FAK-PI3K signaling pathways; and in PC, tenascin-C, semaphorin 3D, as well as the KRAS-induced NF-κB signaling, and the TGFβ-induced, Rho-mediated EMT pathway. This evidence concerns the gene KRAS and gastric cancer.