Under this scenario, specific B-ALL development was observed in 25% (7 out of 28) of Pax5+/− animals (but none of the WT mice) of the early exposure group (Fig. 2b), closely resembling the penetrance of B-ALL development in Pax5+/− mice with delayed exposure3 and in humans harboring a heterozygous PAX5 c.547G>A pathogenic variant22–24. The gene discussed is PAX5; the disease is precursor B-cell acute lymphoblastic leukemia.