Global TEL-AML1-expressing zebrafish B-ALL showed significant down-regulation of endogenous zebrafish tel. This may explain the long latency and low incidence of B-ALL in these fish, as two tel alleles would need to be disabled, rather than one (in human patients, the first TEL is disabled by the translocation itself). This evidence concerns the gene RUNX1 and precursor B-cell acute lymphoblastic leukemia.