160 Gayed: Lifton Figure 1. The accepted genetic map for the region associated with pseudohypoaldostero- nism type 1. (From the NCBI Map Viewer, chromosomal region 4q31.1) regulation. Among them are two forms of type I pseudohypoaldosteronism, Gitelman’s syn- drome, Bartter’s syndrome, glucocorticoid-re- mediable aldosteronism, Liddle syndrome, and pregnancy-induced hypertension (the mecha- nism of which, ironically, was characterized while studying an adolescent boy who suffered from significantly elevated blood pressure). The last three of these diseases all cause hy- pertension, and until recently, physicians could do little more than haphazardly prescribe any number of 70 antihypertensive drugs. Using genomic methods and data, however, Lifton and his colleagues more precisely have de- scribed the distinct and varied genetic causes of hypertension in several diseases. Previous to 1980, it only would have been possible to identify disease genes if such genes encoded protein products that could be purified [2]. Once isolated, fragments of pro- teins were subjected to amino acid sequenc- ing. Scientists then could construct several oligonucleotides that corresponded to all pos- sible codon permutations of the amino acid sequence. The batch of synthesized oligonu- cleotides then could be used to screen a li- brary of expressed genes (cDNA) in hopes of identifying the gene of interest. Now scientists like Lifton use markers unique to a monogenic disease to locate, clone, and study a disease gene. Genetic markers themselves first can be identified by collecting tissue samples from healthy and afflicted family members and then analyzing those samples for specific sequence patterns, such as single nucleotide polymorphisms.