A total of 150 case subjects and 150 control subjects (age-matched within 5 years) will be recruited for this study. This sample size was determined by statistically simulating the study findings 1,000-times using the following assumptions: an alpha level of 0.05; 2-sided hypothesis testing; and an expected distribution across the CC, CT, and TT factor H genotypes of 8.1%, 52%, and 39.9%, respectively, (combining observed data for Caucasians and African Americans [1]). The investigators also assumed approximately 35% of the case and control subjects would be current smokers (see http://www.mit.edu/people/jeffrey/HarrisVARept97.pdf; a report commissioned by the Department of Veterans Affairs Assistant Secretary for Policy and Planning). Finally, the investigators assumed that smoking status in combination with haplotype status had a multiplicative interactive effect on the measurement parameter of interest (i.e., complement protein Ba, D and C3d levels). That is, smoking was allowed to have a negligible impact on the measurement parameter among those in the low-risk genotype, but those in the heterozygous and homozygous risk genotypes had a 1.5-fold and 2-fold greater measurement, respectively. The simulation also included a direct effect of AMD status (case/control), with AMD cases having higher values than controls. Through this simulation process, the investigators were able to show that the sample size of 150 cases and 150 controls would provide 85% power to detect a significant smoking by genotype interaction, the main focus of this study. Note that the investigators' sample size is comparable to similar prior studies, one of which used 112 AMD patients and 67 controls [2], and another that used 274 samples [3] and was conducted by the investigators' collaborator, Dr. Edwards.