The aim of the work was to investigate a possible association of Fcγ receptor IIIA (FcγRIIIA) gene polymorphism at position 158 with the outcome of rheumatoid arthritis (RA). Method: 30 RA patients after being confirmed by routine investigations and 30 unrelated healthy control subjects from the same population were studied. Patients and controls were subjected to genotyping for FcγRIIIA-158V/F using a method based on polymerase chain reaction(PCR) and restriction fragment length polymorphism analysis using amplification created restriction sites (Neito et al, 2000) . Results: The wild type FF genotype was detected in 23/30 (76.7%) of controls and in 15/30(50%) of cases with p value=0.194. Heterozygous mutant gene (FV hetero type) was detected in 7/30 (23.4%) of controls and in 14/30 (46.7%) of cases with p value=0.127. Homozygous mutant gene (VV homo type) was not detected in controls but was detected in 1/30 (3.3%) of cases, p value could not be calculated as the homozygous gene was not detected in the control subjects. On correlating the FF genotype with the non -FF types in both cases and control groups there was p value was 0.042. (OR=0.304, 95%CI, 0.100-0.922). Conclusion: FcγIIIa genotyping revealed that there was no statistical difference between RA patients and controls regarding the FF and FV genotypes. The VV genotype was detected in RA patients but not in the controls. No statistically significant difference was noticed between RA patients with normal or polymorphic FcγRIIIa as regards their age, gender, clinical characteristics and laboratory findings. However on correlating the FF genotype with the non -FF types in both cases and control groups there was a statistically significant difference. This finding might suggest that the FF wild type might have a protective role against RA.