In fetal/neonatal stages, increased Arid3a at the pre-B cell and immature B cell stages as a Lin28+Let7− outcome is crucial for generating B1a cells together with the environment for initial self-ligand reactive BCR selection, B1a cell maintenance, self-renewal throughout life, and the potential for development of CLL/lymphoma in aged mice. The gene discussed is ARID3A; the disease is B-cell chronic lymphocytic leukemia.