CD7 is a transmembrane glycoprotein expressed on T cells and natural killer cells that serves a costimulatory role in immune activation. Upon binding to its ligand K12/SECTM1, CD7 promotes T-cell activation and mediates cytokine production including interleukin-2, while activation on resting NK cells induces interferon-gamma secretion. CD7 is highly expressed in acute T-cell leukemia and peripheral T-cell lymphomas, making it a prominent target for immunotherapy. Multiple clinical trials have demonstrated the safety and efficacy of CD7-directed chimeric antigen receptor (CAR) T-cell therapy for relapsed/refractory T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma, with complete remission rates of 81–90% in bone marrow 1 2 3. Engineering strategies—including genetic disruption of the CD7 gene in CAR T cells, naturally selected approaches that mask CD7 epitopes, nanobody-derived fratricide-resistant designs, and pharmacologic inhibition of CAR signaling—have been developed to overcome self-targeting of CD7 CAR T cells against normal CD7-positive lymphocytes 4 1 5. Clinical toxicity is generally manageable, with cytokine release syndrome and transient cytopenias predominating 6. Emerging approaches include CAR-NK cells and extracellular vesicle-based delivery systems targeting CD7 7 8.