We found that c-myb alternative splicing is greatly increased in precursor B-ALL samples, that the pattern of c-myb alternative splicing is more complex in leukemia patients than in normal CD34+ cells, and that the pattern is distinct in each patient sample, suggesting that activation of alternative RNA splicing is a mechanism that could contribute to leukemogenesis. The gene discussed is MYB; the disease is acute lymphoblastic leukemia.