Likewise, recurrent genomic deletions in B-ALL have been associated with aberrant RAG1 activity by others because of the presence of cryptic RAG1 cleavage sites at individual deletion breakpoints (Holmfeldt et al., 2013, Iacobucci et al., 2009, Mullighan et al., 2008). This evidence concerns the gene RAG1 and precursor B-cell acute lymphoblastic leukemia.