Likewise, Zhou et al. have described an aberrant functionality of DCs in adult B lineage ALL [38] and Mami et al. [37] were not able to generate CD1a+ myeloid or ILT3+ plasmacytoid DCs from circulating CD34+ precursor cells of ALL patients, suggesting that DC differentiation was altered in B cell precursor ALL. This evidence concerns the gene CD1A and acute lymphoblastic leukemia.