KIF23 and gastric cancer: These pathways play critical roles in cell proliferation, metabolism, differentiation, invasion/metastasis, and survival.[26–28] In gastric cancer, KIF23 facilitated cell proliferation through directly binding with APC membrane recruitment 1 (Amer) to activate the Wnt/β-catenin signaling pathway.[29] In our study, results of GSEA suggested that DLBCL patients with KIF23 higher expression showed activation of PI3 K/AKT/mTOR, TGF-β, and Wnt/beta/catenin signaling pathways.