A new review maps how cold agglutinin disease is defined by clonal B-cell biology and complement-mediated hemolysis, and it summarizes why older approaches such as steroids and splenectomy have often underperformed. The article also positions sutimlimab as a central therapy within a changing treatment landscape. Rather than treating cold agglutinin disease as a single phenotype, the review emphasizes how the underlying mechanism shapes treatment response and tolerability, and it highlights the emergence of additional agents designed to build on complement inhibition. The publication frames care around the biologic driver—complement activation—while acknowledging gaps in how therapies compare across patient subgroups. For drug developers, the analysis underscores that mechanism-based sequencing and combination strategies remain key areas for clinical refinement in a disorder where effective disease control can substantially improve anemia-related morbidity and patient quality of life.