There is a large body of in vitro, animal, and now human data that provide strong support for PAF as being an important mediator of asthma and airway hyperreactivity. Unfortunately, there is little direct, unequivocal evidence that this is so. Direct evidence will come from studies that test the effectiveness of potent, nontoxic, PAF receptor antagonists in patients with asthma. Another issue that needs to be addressed is the mechanism by which PAF produces bronchoconstriction and, in particular, airway hyperreactivity. Studies exploring the effect of PAF on inflammatory cell populations and functions in the lung, on other mediators (i.e., leukotrienes), and on the nonadrenergic, noncholinergic nervous system in human subjects are needed. Finally, identification of the basis for the variable response to PAF in normal subjects and in patients with asthma should provide further insight into PAF's mechanism of action and the pathogenesis of asthma and airway hyperreactivity.