Tuberculosis, a chronic infectious disease caused by Mycobacterium tuberculosis, has reemerged as a leading public health problem. Approximately one-third of the world’s population is infected with M. tuberculosis, and a recent World Health Organization report estimated that, in 1998, there were 8 million new cases of clinical tuberculosis and 1.9 million deaths from the disease. Interestingly, not all individuals exposed to M. tuberculosis become infected. Moreover, progression toward clinical tuberculosis is far from an inevitable consequence of infection with M. tuberculosis, since only∼ 10% of the vast number of infected individuals actually develop clinical disease (Bloom and Small 1998). Both M. tuberculosis infection and clinical tuberculosis result from complex interactions between the infectious agent, environmental factors, and the host. The involvement of human genes in tuberculosis has been suggested by numerous epidemiological observations. Several studies have shown that a person’s resistance level to M. tuberculosis infection correlates with the region of his or her ancestry and that the ancestors of more-susceptible persons tend to come from areas once free of tuberculosis (Stead 1992). Similarly, the incidence of clinical tuberculosis has been found to be particularly high during outbreaks in populations, such as that of Native Americans, with no ancestral experience of the infection (Stead 1997). Twin studies have also demonstrated the importance of host genes, by showing higher concordance rates for clinical tuberculosis among MZ than among DZ pairs (Comstock 1978).