Sda or SID1, the only antigen of the SID blood group system, was discovered in 1967. About 90% of the European population carries the antigen on their red blood cells (RBCs). Although there are 10% missing the antigen on their RBCs only 4% lack expression in all tissues and fluids and thereby have the true null phenotype, Sd(a-). The antibodies against Sda form a characteristic RBC agglutination pattern of small agglutinates surrounded by numerous free cells. The B4GALNT2-encoded transferase synthesizes the Sda antigen by the addition of an N-acetylgalactosamine to its precursors, which can be glycans on glycoproteins or glycosphingolipid conjugates (in the neolacto synthetic pathway). Alterations in B4GALNT2 that abolish transferase activity cause the Sd(a-) phenotype. Another phenotype, the rare Cad or Sd(a++) or Super-SID, describes RBCs that are more strongly agglutinated by anti-Sda. If this trait is quantitative or qualitative is to date not fully understood, nor is its genetic background. Differences from reference allele SID*01 (accession number AJ517770) are given in the table.