B cell development is often portrayed as a series of decision points that expand an antigen-reactive cell to a clone producing a single antibody. This is hardly the case: B cell development is dependent on a series of error-prone, random rearrangement events that through ongoing diversification reach a compromise in which most cells are not autoreactive (except in disease) and the majority of clone members remain specific for the initial antigen. One familiar example of ongoing diversification is somatic mutation during clonal expansion (1). Another example, receptor editing, is the means by which immature bone marrow B cells become self-tolerant (2–4). Here rearrangements are induced by encounter with autoantigens to change specificity from self to non-self. Now, a third level of diversification, termed “receptor revision,” has been suggested to occur in mature B cells. Initial evidence for revision included recombination activating gene (RAG) expression in germinal centers along with attendant double-stranded breaks adjacent to recombination signal sequences (RSS)(5–7), but the strongest evidence comes from examples of cells that underwent revision after somatic mutation was initiated. The paper in this issue by Wilson et al.(8), along with two previous studies (9, 10), identifies clones of B cells that include cells whose antibody genes have undergone concurrent mutation and revision. These findings place receptor revision firmly into the environment of germinal centers. In addition to somatic mutation, this is where other important immunological processes happen, including H chain class switch and immune memory formation. The germinal center cell subset that expresses most RAG activity appears to be the noncycling, centrocyte cells (5, 11). Unlike other peripheral B cells, these cells express many markers shared by bone marrow B cells, including surrogate L chain components, IL-7R, and in humans, terminal deoxynucleotidyl transferase (6, 11, 12). Furthermore, purified IgD splenic B cells express RAG upon exposure either to a combination of CD40 antibodies and IL-4 (agents that are thought to mimic T cell help), or to a combination of LPS and IL-4 (7). More recent studies show that IL-7, rather than IL-4, may be the critical cytokine driving receptor revision in vivo since RAG expression is unperturbed in the germinal centers of immunized IL-4–deficient mice, but is blocked in anti–IL-7R–treated mice (12). Interestingly, IL-7 is also a key cytokine for immature B cell expansion. These parallels between the cells undergoing receptor revision and immature B cells supported the idea that germinal center B cells reinduce a gene expression program characteristic of less mature cells, a concept known as “neoteny”(5). Reprogramming might be initiated by a lethal mutation in VH or VL. Such a mutant might resemble a pro-B or pre-B cell, and other phenotypes such as RAG expression might be activated. The similarities between RAG-expressing bone marrow and germinal center B cells raise the possibility that receptor editing is going on in immature B cells that have migrated to the periphery. Three recent papers examining RAG indicator mice (13–15) reinforce this concern. Nussenzweig and colleagues generated bac-transgenic mice expressing a green fluorescent protein (GFP) gene placed in the context of 100 kb of the RAG gene cis-acting elements (13). Here, the cells expressing GFP in the periphery had the phenotype of newly minted bone marrow B cells, not germinal center cells. Furthermore, stimuli that were thought to increase RAG expression in vitro or in vivo failed to demonstrate upregulation of GFP and may just have prolonged …