Conversely, mice lacking Sox4 have shown pro-B-lymphocyte expansion and defects in cardiac outflow tract formation.24 Furthermore, a previous study that employed retroviral transduction of Sox4 and bone marrow transplantation techniques revealed that increased Sox4 expression may cooperate with the deregulation of Mef2c expression to induce myeloid leukemia in recipient mice.25 The gene discussed is SOX4; the disease is myeloid leukemia.