Immune heparin-induced thrombocytopenia (HIT) is a common adverse event in certain patient populations who receive standard, unfractionated heparin (UFH) for one week or more, such as postoperative patients (1). Describing this reaction as “common” or “frequent” is not an exaggeration: according to the Council for International Organization of Medical Sciences (2), an adverse drug effect seen in 1% or more patients is common (or frequent). In contrast, reactions that occur in 0.1 to 1% of patients are termed “uncommon” or “infrequent,” and those affecting 0.01-0.1% and <0.01% are “rare” and “very rare,” respectively. HIT is caused by immune mechanisms and paradoxically is associated with thrombosis. The unusual prothrombotic character of HIT results from in vivo thrombin generation that results when antibodies are generated against a “self” molecule [platelet factor 4 (PF4)] that has undergone conformational modification in the presence of heparin. In recent years, emphasis has shifted towards treatment and prevention of HIT-associated thrombosis by non-heparin anticoagulants, and also to delaying therapy with oral anticoagulants because of the risk of warfarin-induced microvascular thrombosis. Recently, interest in preventing HIT or its complications has increased, using strategies such as targeted platelet count monitoring and considering use of heparin (and related) preparations that are less likely to cause this immune reaction. Recent reviews highlight these and other aspects of HIT (3-5).