The human Rhesus genes RHD and RHCE are two closely linked genes in a two-locus system encoding for the D and the CcEe blood group antigens. The Rh blood group is a polymorphic system with significant issues in blood transfusion. This holds especially true for Rhesus D (RhD). Genotypes derived from gene conversion, polymorphism and mutation are responsible for the synthesis of polymorphic proteins such as weak D, partial D, and DEL phenotypes. The identification of D variants is important in cases of transfusion or pregnancy because RhD-negative patients and patients with D variants are in danger of immunization by RhD-positive blood cells. Serologic RhD typing is often uncertain because monoclonal anti-D reagents may or may not react with weak and partial D types. The behavior of reagents with D variants is not consistent even within a certain Rhesus cluster such as DAU. We learned that variants are able to react as strong as normal RhD-positive erythrocytes with monoclonal antibodies while others react weak, faint or with no detectable agglutinations. In a pregnant case with later on proven RHD*10 (DAU) and categorized as partial D, we were close on false RhD phenotyping because all serologic tests resulted in full strength reaction with several different anti-D reagents in different standard tests. At no time, agglutination signs for a weak or partial D variant have occurred. This case marks a perfect example for dangerous errors in the serology of RhD phenotyping that could have had unwanted consequences in the omission of appropriate anti-D prophylaxis, or in general terms, in possible transfusion situations. The DAU cluster and other genetic RHD variants may be rare in the European population, while certain D variants are more frequent in some ethnicities than in others. The possibility of false results in D antigen typing is never to rule out since D variants are prone to be undetected by serologic testing. The correct determination of the RhD status is only done by molecular analysis.