Anti-D (-RH1) of the Rh blood group system is clinically important as it causes haemolytic transfusion reactions and haemolytic disease of the fetus and newborn. Although most people are either D+ or DÀ, there is a plethora of D variants, often categorized as either weak D or partial D. These two types are inadequately defined and the dichotomy is potentially misleading. DVI is the D variant most commonly associated with anti-D production and UK guidelines recommend that patients are tested with anti-D reagents that do not react with DVI. Weak D types 1, 2, and 3 are seldom, if ever, associated with alloanti-D production, so a policy recommendation would be to treat patients with those D variants as D+, to preserve DÀ stocks, whereas patients with all other D variants would be treated as DÀ. All donors with D variant red cells, including DVI, should be treated as D+. The frequency of the D+ phenotype is about 85% in Caucasians, around 95% in sub-Saharan Africa, and greater than 99Á5% in eastern Asia (Daniels, 2013). Although most people are either D+ or DÀ, a grey area exists in the form of a plethora of D variants: the so-called weak D, partial D, and DEL phenotypes. These ill-defined terms are often a cause of consternation beyond their clinical relevance. Over its history of well over a century, blood group serology has been fraught with problems arising from nomenclature, and the terminology applied to D variants has led to confusion.In this review I will attempt to clarify the situation, recommend a testing and transfusion strategy that minimizes the risk of alloimmunization without undue waste of DÀ blood stocks, and describe the clinical issues relating to these aberrant forms of D.