The overexpression of RAB5C in this B-ALL subset, along with our findings that RAB5C supports growth of B-ALL cells, suggests that RAB5C may represent a target for treatment of the TEL/AML-1 B-ALL subset, especially if future studies reveal that growth of primary B-ALL cases harboring TEL/AML-1 is highly dependent on RAB5C. Here, RUNX1 is linked to precursor B-cell acute lymphoblastic leukemia.