Childhood leukemia is a genetically and phenotypically heterogeneousdisease. However, there are significant progresses in identifying mutantgenes that are causally implicated in disease pathogenesis. These insightsin turn have generated strategies for improving treatment outcome andminimizing toxicity of therapies. (Gilliland and Tallman , 2004). Since 1970, the cure rate of acute lymphoblastic leukemia (ALL) inchildren has increased dramatically, from less than 30 percent toapproximately 80 percent. This remarkable improvement has resultedfrom the marriage of laboratory and clinical science. The identification ofeffective agents in randomized cooperative-group studies, the applicationof treatment to the central nervous system before the onset of symptoms,the intensification of treatment, and the use of "risk-adapted therapy"(therapy tailored to the predicted risk of relapse) have led to today'simpressive cure rates. ( Naomi , et al ; 2004). Despite these successes, however, much work remains. Many of thechildren with ALL who are cured by current therapies are overtreated andthus unnecessarily exposed to the risk of short- and long-term adverseeffects. ( Margolin, et al ; 2006). A risk-adapted stratification scheme emerged from the identification ofclinical and laboratory variables unique to the host or leukemic blast thatare predictive of the outcome. Age and white-cell count at diagnosis, sex,and immunophenotypic and cytogenetic differences among lymphoblastpopulations can be used to tailor therapy so that the chances of cure aremaximized while exposure to unnecessary risk is minimized. (Carroll, et al ; 2003 ). Risk-based treatment assignment requires the availability of prognosticfactors that reliably predict outcome. For children with ALL, a number ofclinical and laboratory features have demonstrated prognostic values (Pui et al, 2001) (Pullen et al, 1999). Molecular genetic studies serve a variety of roles in the evaluation ofhematopoietic tumors, including clarification of the precise molecularlesion of a detected karyotypic abnormality, identification of occultcytogenetic aberrations , detection of gene rearrangements that do not cause identifiable karyotype changes , and detection of minimal residualdisease (Daniel, et al, 2006). The extent of clearance of leukemic cells from the blood or bone marrowduring the early phase of therapy becomes an independent prognosticfactor in acute lymphoblastic leukemia (ALL) (Jacquy et al 1997). MRD analysis has a powerful prognostic factor in both first line andrelapse treatment, actually it plays a useful role in the risk directedtreatment of childhood ALL (Moppett et al, 2003). It may allowsidentification of true low-risk and high-risk patients, who may profit fromtreatment reduction or treatment intensification, respectively (Velden etal, 2004). In fact MRD reflects both the drug responsiveness of leukemiccells and host pharmacodynamics / pharmacogenomics and is the mostreliable prognostic indicator for gauging the intensity of treatment (Pui2004).