Receptor editing has emerged from its original identification as a minor secondary mechanism of B cell tolerance to be considered as a dominant mechanism by which autoreactive immature B cells are rendered tolerant. Clonal deletion, previously regarded as the major mechanism of central B cell tolerance, has been shown by recent studies to operate secondarily and only when receptor editing is unable to provide a non-autoreactive specificity. Receptor editing has also been shown to operate during the development of wild-type B lymphocytes, and ongoing investigations demonstrate the influence of particular signaling molecules in the induction and/or inhibition of receptor editing. Together, these studies begin to map the signaling pathways that regulate receptor editing in autoreactive and non-autoreactive immature B cells.