Abbas and colleagues showed that BCL11B overexpression in 32D myeloid cell line resulted in a decreased proliferation, less maturation toward granulocyte and more undifferentiated blast cells [40], but did not detect a transforming ability of BCL11B. Thus, further studies are needed to clarify the role of and interplay between the chimeric protein and co-occurring alterations in acute leukemia in an effort to identify potential therapeutic targets for these patients. The gene discussed is BCL11B; the disease is acute leukemia.