In TNBC and HCC, cancer cells would exhibit more aggressive phenotypes partially attributed to CXCL13-CXCR5 interactions in autocrine (to enhance self-renewal and survival through CXCL13 production and CXCR5 upregulation), paracrine (to induce proliferation and invasion signal for adjacent cancer cells) or endocrine (to facilitate pre-metastatic niche formation at distant sites) manners. The gene discussed is CXCR5; the disease is cancer.