genes may actually be involved in each disease it is impractical to identify more than a dozen new drug targets for each disease given the cost of new drug development and the limited number of research pharmaceutical companies the first approach to finding additional snps will be computational an additional 500 nucleotides will be added to both the 5 u2032 and 3 u2032 ends of each tfc and promoter and this wider net used to troll for additional snps these snps are expected to be in linkage disequilibrium with the tfc or 5 u2032 or 3 u2032 region in question and makes it possible to include these regions without the need to do additional snp discovery these additional snps will make up chip 1a and chip 2a if use of the additional snps derived computationally is still insufficient to find strongly disease associated snps then selected tfc and promoter regions will be amplified and sequenced directly to find snps snps obtained by direct sequencing of tfcs will constitute chip 1c promoter snps obtained by sequencing will make up chip 2c thirty samples are pooled and snps used whose peak height exceeds 20 of the majority peak marth et al nat genet 1999 december 23 4 452 6 start with 100 regulatory region snps either derived from tfc 39 s or 5 u2032 regions using control dna demonstrate reproducible reliable genotyping at these 100 loci for one dozen different control individuals next expand to 6 000 10 000 snps chip 1 demonstrate reproducible snp typing for one dozen control samples ie genotype 12 samples using 6 different chips compare the results for each chip 2 using a single disease e g sporadic.