On the basis of the concurrent overexpression of MYCN and TAL1 detected in a large proportion of blast cells from pediatric T-ALL samples, along with the evidence in qRT-PCR analysis that TAL1 knockdown resulted in a reduction on MYCN expression and that TAL1 directly binds to MYCN promoter region by ChIP analysis, we hypothesized that TAL1 pathway activation could directly sustain the up-regulation of MYCN expression. This evidence concerns the gene MYCN and acute lymphoblastic leukemia.