At the immature B cell stage the BCR signals the down-regulation of the RAG genes and Ig L chain (LC) allelic and isotype exclusion. The signaling pathway that regulates these events is poorly characterized. We demonstrate that immature B cells from mice deficient in the PI3K catalytic subunit p110δ fail to suppress RAG expression and inappropriately recombine κ and λ LC loci. In addition, in the presence of the autoantigen, clonal deletion and receptor editing still takes place, demonstrating that these processes are independent of p110δ. These results demonstrate a role for p110δ in the regulation of RAG gene expression and thereby LC allelic/isotype exclusion.