“…They observed three phenotypes A D A 1, A D A 2-1, and A D A 2, which were controlled by two codominant alleles A D A * I and ADA*2. Subsequently, several rare variants were identified and shown by family studies to represent heterozygous combinations of either A D A * I or ADA*2 with a rare variant allele (ADA*3, ADA*4, ADA*5, ADA*6, or ADA*7) at the same locus [1,[4][5][6]10].…”