Although more cases are needed to disclose the underlying biological mechanisms responsible for the extreme hyperleukocytosis observed in our T-ALL pediatric case with t(7;19)(q35;p13) and additional submicroscopic deletions at 4q25, 7q33 and 10q23, we cannot rule out that deletions of PTEN or LEF1 genes or other genes in the deleted regions may have influenced to the aggressive course in concert with the elevated LYL1 expression. The gene discussed is PTEN; the disease is acute lymphoblastic leukemia.