Sachais et al describe small molecule inhibitors that dock to platelet factor 4 (PF4) at sites that are critical for multimerization and, at micromolar concentrations, promote dissociation of PF4 tetramers into dimers and monomers. If these agents act similarly in vivo, they could provide a means of preventing and disrupting the immune complexes that are central to heparin-induced thrombocytopenia (HIT) pathogenesis. Professional illustration by Kenneth X. Probst.