For typing of the RH system, 120 RHD-negative and 30 RHD-positive donors were selected as one of the aims of the study was to elucidate the risk of obtaining false-positive results in D-negative donors. All 150 samples were typed correctly by the intron 4 assay [12], thus excluding a high frequency of either the RHD pseudogene [7] or any other unexpected molecular basis with grossly intact RHD genes accounting for RHD negativity in the Jordanian donors. In addition, the RHD pseudogene was not found among the RHD-positive samples when screened with an assay specific for the characteristic 37-bp duplication. For a more detailed analysis of both RHD and RHCE polymorphisms, another method was utilized [13]. Ninety samples (80 RHD negative and 10 RHD positive) were analysed. Of the 80 RHD-negative samples (one r’r’, three r’r and the others rr), all but one typed negative for RHD markers tested in exons 2–7, 9 and 10. A single sample (r’r) was positive for the RHC markers in primer mixes 1 and 9, but also in mix 8. The RHD-specific primer in this mix reacts with nt 1255 in exon 10. The RHD specificity of the 3′ end of this RHCE gene was confirmed by a positive reaction with another method [22]. The 10 RHD-positive samples were positive for all eight RHD exon markers in this assay. RHCE typing gave concordant results except in two cases – one RHD positive (Ro) and one RHD negative (rr) – where false-positive reactions corresponding to the well-known c(cyt48) variant were noted. However, a method for detection of the intron 2-specific RHC insertion [23] was negative, as expected. This test was positive in the four r’r’ and r’r samples mentioned above. Representative RH genotyping results are shown in Fig. 1. Owing to the mode of selection of blood donors for RH typing, no allele frequencies were estimated.