Attempts to substitute this polyclonal anti-RhD IgG prophylaxis with RhD-specific monoclonal IgG Abs have failed because the monoclonal RhD-specific IgG Abs were relatively unstable due to intramolecular rearrangements or did not clear RhD-positive RBCs as rapidly as the available polyclonal anti-RhD IgG Abs inin vitro assays or clinical trials and/or did not sufficiently inhibit allo-immunization in clinical trials1,4,8. This evidence concerns the gene RHD and rheumatic heart disease.