Although the mechanism as to how CXCL-13 participates in 5-FU resistance was not stated, it is highly plausible that resistance is achieved through piggybacking the same pathways responsible in promoting tumor growth, migration, and invasion in CXCR5-expressing colon cancer cells; through the activation of PI3K/AKT/mTOR and Wnt/β-catenin signaling pathways [112,146,147]. The gene discussed is AKT1; the disease is colonic neoplasm.