The Rh blood group system is the most polymorphic of the human blood groups, consisting of at least 50 independent antigens and, next to ABO, is the most clinically significant in transfusion medicine (Avent & Reid, 2000). The D antigen is the most immunogenic antigen of the Rh system. About 18% of Caucasians do not express an antigen D (Rh negative) and most Rh-negative cases are caused by RHD gene deletion. About 0.2-1 % of Caucasians have red blood cells with reduced expression of the D antigen (Lin et al., 2003). The antibodies in the Rh blood group system can cause severe transfusion reactions and are second only to the ABO system in this regard. Blood grouping by serology has been an enormously successful technology which has made transfusion safe. But the experts in the field are well aware that blood incompatibility remains a significant problem in transfusion medicine and that these problems reflect certain inherent limitations of hemagglutination based testing (Antonella et al., 2009). The molecular genetics world was revolutionized in 1983 with the advent of PCR (polymerase chain reaction), which allows the amplification of DNA and analysis of genes. The molecular identification and characterization of blood group genes revealed that the majority of clinically important blood group antigens are encoded by SNPs (Daniels, 2009). The aim of this study is to investigate the role of RHD molecular typing technique in solving RHD typing discrepancies during routine testing due to partial D or weak D phenotypes. Compare currently used serologic methods with molecular analysis to determine the potential application of molecular methods to improve RHD typing strategies.