In agreement with this finding, our studies show that, in Pax5+/− mice, immune training by early exposure to infection does not have a protective effect against the conversion of the preleukemic clone into B-ALL, therefore conflicting with the “delayed infection” hypothesis for this specific molecular subtype of B-ALL, and instead supporting Kinlen’s “population mixing” explanation for the epidemiological findings. The gene discussed is PAX5; the disease is infection.