A family study of 2 parents and 5 SD identical (HLA-A1, A3, B7, B8) siblings, one of whom has ‘classic CAH’ has been used to demonstrate that in this family the maternally inherited HLA-B8 antigen is not solely serving to mark genetic predisposition to this disease. The patient’s lymphocytes both responded to, and stimulated those of her 4 siblings in MLR indicating the possible involvement of an HLA-D antigen in CAH. This HLA-D antigen could have been of paternal origin, or could have been a result of a recombination event involving an HLA-D antigen linked to the maternal HLA-A2, B12 haplotype. The lymphocytes of the four healthy siblings were mutually unresponsive i