CXCR5 and neoplasm: CXCL13 acted specifically to recruit and position CXCR5+ cells in lymphoid follicles, primarily CXCR5+ B cells.[39] Overexpression of CXCL13 in an inflamed tissue appeared to promote the formation of functional TLSs, and activate humoral anti‐tumor response.[40]IL‐21 produced by TFH cells played an important role in B cell proliferation, activation, and differentiation.[41] HAIC treatment exhibited the ability to reshape B cell plasticity and promote TLS formation, as evidenced by the increased density of CD20+ B cells and TLSs in post‐HAIC tumors.