Genome wide association studies have identified marker polymorphisms at more than 80 new susceptibility loci for breast cancer, including ESR1. Several of these loci are associated with risk of both estrogen-negative breast cancer and serous ovarian cancer, providing further evidence of their common etiology; others are also associated with mammographic density, and with breast size. Identifying the genes targetted by these polymorphisms is likely to reveal novel pathways to tumorigenesis, and provide new opportunities for breast cancer prevention through drug repositioning and development. However, in order to do this is it necessary to go beyond identifying the marker polymorphisms to fine mapping the associations in large sample sizes in order to find the candiate causal polymorphisms, and then to determine their function and target gene(s) through multiple approaches including expression quantitative trait analysis, chromatin conformation capture and luciferase assays. Our experience todate has shown that there are often multiple independent sets of correlated, highly trait-associated variants clustered in a genomic region, and that the causal polymorphisms in these iCHAVs can target multiple genes in the region. Although only a handful of the known breast cancer susceptibility loci have been examined in any detail, we are already finding many surprises in terms of the target genes, and the expression levels associated with breast cancer risk. I will illustrate these issues by discussing the fine mapping and functional analysis of several loci identified by the Breast Cancer Association Consortium.