Since the Rag1 negative pro-B cell arrested population in our model is highly susceptible to IL-7 exhaustion and subsequent cell death, disruption of IL-7R signaling could enable the Aid expression necessary to clear Rag1 deficient pre-leukemic clones, which would be a mechanistic explanation for the dose-dependent pro-B ALL acceleration in Aid deficient counterparts. This evidence concerns the gene IL7R and acute lymphoblastic leukemia.