Cxcr4, also known as fusin or CD184, is a 7-transmembrane helix G-protein-coupled receptor encoded by the Cxcr4 gene. It plays a central role in various physiological processes, such as cell migration, hematopoiesis, cell homing and retention in the bone marrow. It forms an interaction with its endogenous partner, chemokine ligand 12 (CXCL12, also named SDF-1), and this CXCR4/CXCL12 couple is involved in numerous signaling pathways that are crucial for normal biological functions as well as disease development [1].

The CXCR4/CXCL12 axis has been extensively studied in the context of diseases. In malignancies, overexpression of CXCR4 in tumor tissues is highly correlated with tumor aggressiveness, metastasis and recurrence, across various cancers like breast, gastric, non-small cell lung cancer, and gastrointestinal cancers [1,4]. In glioblastoma, the receptor is associated with cancer stem cell biology, resistance to chemo-and radiotherapy, and tumor angiogenesis [2]. In hematological malignancies, CXCR4 overexpression drives disease progression, boosts tumor cell survival and promotes chemoresistance [5]. Moreover, in non-oncologic settings, CXCR4 is involved in inflammatory diseases, and its targeting can potentially improve the detection of primary aldosteronism and atherosclerotic disease [3].

In conclusion, Cxcr4 is a key player in multiple biological processes and disease conditions. Through research, its role in promoting tumor growth, affecting disease prognosis in malignancies, and contributing to inflammatory and other non-oncologic diseases has been revealed. Understanding Cxcr4's functions, especially through model-based research, may offer new therapeutic strategies for these diseases.