We show that the set of initiating autoantibodies is usually limited to Ro, nRNP A, phospholipids and rheumatoid factor of the specificities tested, suggesting that there appears to be an autoantigentic bottleneck that restricts autoantibody initiation to a relatively small number of initial antigenic structures on the pathway to SLE development. The gene discussed is CALR; the disease is systemic lupus erythematosus.