Microvascular inflammation (MVI) is a hallmark of antibody-mediated rejection (AMR) and an important predictor of long-term allograft outcomes in kidney transplantation. This symposium examines the clinical significance of MVI, including its association with graft injury and loss1, and reviews the impact of current standard treatments and investigational therapies on MVI. The session highlights CD38⁺ cells as central drivers of antibody-dependent and -independent mechanisms of MVI, with a focus on the role of activated CD38⁺ natural killer (NK) cells2,3. These findings provide rationale for CD38-targeted therapies as a potential strategy to modify the underlying biology of AMR and MVI. We examine clinical evidence supporting this approach, including data from the Phase 2 felzartamab study and subsequent open-label extension evaluating the effects of targeting CD38 on AMR activity, biomarkers, and molecular features of disease over time. Biogen 291974 Disclaimers: Felzartamab is investigational and is not approved for use in any country. The safety profile and efficacy has not yet been established. BIOGEN is a registered trademark of Biogen MA Inc. Biogen Australia Pty Ltd, Macquarie Park, NSW. ABN 30 095 760 115. Date of preparation: July 2026. © 2026 Biogen. All rights reserved. References: 1. Sablik M, et al. N Engl J Med. 2025;392(8):763-776. 2. Heeger PS, et al. Nat Rev Nephrol.2024;20(4):218-232 3. Pontrelli P, et al. Front Immunol. 2020;11:1454