The clonal selection theory postulates that immune tolerance mediated selection occurs at the level of the cell. The receptor editing model, instead, suggests that selection occurs at the level of the B-cell receptor, so that self-reactive receptors that encounter autoantigen in the bone marrow are altered through secondary rearrangement. Recent studies in transgenic model systems and normal B cells, both in vivo and in vitro, have demonstrated that receptor editing is a major mechanism for inducing B-cell tolerance.