Wilms’ tumor gene (WT1) was first reported as the gene responsible for Wilms’tumor, a pediatric renal cancer. Constitutive expression of wild type or mutant WT1has been demonstrated in blasts of nearly all acute leukemias irrespective of lineagespecificity. Therefore, WT1 expression may be regarded as a nonspecific"panleukemic" molecular marker. WT1 transcription is regulated in erythroid andmyeloid lineages by the transcription factor GATA1. The aim of this study was toinvestigate the expression of WT1 and its transcription factor GATA1 in untreatednewly diagnosed and relapsed acute leukemia patients and to assess the prognosticimpact of this expression on the clinical outcome. In this study, WT1 and GATA1genes expression were analysed using Reverse Transcriptase Polymerase ChainReaction (RT-PCR) in 50 leukemic patients [acute lymphoblastic leukemia (ALL),acute myeloid leukemia (AML)] and 15 healthy controls. The patients were followedup for two years and the probability of overall survival was determined. WT1 geneexpression was significantly higher among leukemic group compared to controls. Itwas found that WT1 gene was expressed in 68% and 76% of ALL and AML patientsrespectively. Relations between WT1 gene expression and prognostic parameterswere done revealing insignificant relations except for higher WT1 gene expressionand unfavorable post induction response including induction failure, partial remission,or death in ALL patients. GATA1 gene was expressed in 48% of ALL patients and60% of AML patients which was significantly higher compared to controls. Relationsbetween GATA1 gene expression and prognostic parameters were also done revealinginsignificant relations except for higher GATA1 gene expression and presence ofthrombocytopenia in ALL patients. Our study demonstrated that 48% of leukemicpatients coexpressed WT1 and GATA1 genes. By follow up, it was found that therewas a highly significant relation between the coexpression of WT1 and GATA1 genesand unfavorable outcome with a significant reduction of survival regarding survival ofpatients expressing either WT1 or GATA1 genes. Our results support the presence ofregulatory interaction between WT1 and GATA1 genes that may result in cellularproliferation and / or differentiation of acute leukemias.