Airway hyperresponsiveness is a key characteristic of human asthma and a marker for asthma–like conditions in animals. F₁ mice derived from A/J and C57BL/6J display a phenotype which resembles the asthma–like phenotype of the A/J mice. Since airway responsiveness failed to segregate as a mendelian trait, we show significant linkage at two loci, Bhr1 (lod = 3.0) and Bhr2 (lod = 3.7) on chromosomes 2 and 15. A third locus, Bhr3 (lod = 2.83), maps to chromosome 17. Each of these loci maps near candidate loci implicated in the pathobiology of asthma. Our study represents the first linkages established through a genome–wide survey of airway hyperresponsiveness in any mammal.