The resistance to cytosine arabinoside (AraC) chemotherapeutic agents is the major problem in the treatment of acute leukemia. The objective of this thesis was to evaluate the effect of genetic alteration of two important genes encoded in the AraC metabolizing enzyme; the deoxy cytidine kinase (dCK) gene with two single nucleotide polymorphisms (SNPs) -360 C>G, -201 C>T and the cytidine deaminase (CDA) gene with two SNPs; 79 A>C, 208 G>A. They were evaluated for genotypes using the RFLP and ARMS PCR techniques and for mRNA expression using the quantitative Real time PCR technique. We performed 94 peripheral blood tests on children with acute lymphoblastic leukemia (ALL) and 100 blood tests on a normal control group from the general population. All genes have 3 possible genotypes; either wild, heterozygous, or variant. The dCK (-360 C>G,-201 C>T) gene in the ALL test group was composed of 72%, 27% and 1% respectively, while the normal control group was composed of 70%,26% and 4% , respectively. The CDA gene, 79 A>C in the ALL test group was composed of 87%,13% and 0%, respectively while the normal control group was composed of 81%,18% and 1%, respectively. The CDA 208 G>A had only one genotype which was 100% wild type. The mRNA expression was studied using a quantitative Real time PCR technique on 44 RNA extracted from bone marrow of recently diagnosed ALL subjects, and calculated using the 2^(-ACT) formula. We found that there was an association between genotypes and toxicity in ALL patients with heterozygous and variant genotypes (-360 CG/-201 CT,-360 GG/- 201 TT) in that there was an AraC related mucositis occurring. However, there was no significant association of AraC toxicity in the alleic genotype of CDA, but this gene was connected to the improvement of patients. It showed that there was an association between Mininmal Residual disease (MRD) and mRNA expression. Neither the genes nor the genotypes were significantly associated with mRNA expression. In conclusion, the results of this study indicated that dCK and CDA were important genes in AraC metabolization.