Transcriptional regulation of the RAG locus has been studied by monitoring RNA levels in sorted cells and by using various green fluorescent protein (GFP) reporter mice. One group generated transgenic mice carrying an artificial V(D)J recombination substrate that activates GFP expression as a consequence of RAG activity [11]. GFP expression persists in this case regardless of ongoing RAG transcription. Three other groups generated RAG transcription reporter mice. One group used gene targeting to generate a RAG2-GFP fusion protein [12], a second group used a bacterial artificial chromosome (BAC) transgene encoding GFP in place of RAG2 [13], and a third group replaced RAG1 with GFP by gene targeting [14,15]. Each of these systems demonstrated similar RAG expression patterns. The three latter groups concluded that RAG is not expressed and cannot be reinduced in RAG-negative mature B cells as had been previously suggested [16–18]. However, other studies continue to suggest that the RAGs can be reactivated leading to “receptor revision” in mature lymphocytes. [19,20]. In humans, RAG expression has also been reported in mature B cell subsets [21] and can be induced by IL-6 [22]. This area remains controversial.