“…Overall, the data suggest that  2 -AR polymorphisms, especially Arg16Gly, may play a role in airway hyperresponsiveness, bronchodilator sensitivity and response to -agonist, long-term use of -agonist, and tolerance (Table 11) Martinez et al, 1997;Tan et al, 1997;D'Amato et al, 1998;Kotani et al, 1999;Fowler et al, 2000;Israel et al, 2000;Lima et al, 2000;Taylor et al, 2000a). Future studies will need to identify individuals at risk for the development of asthma in addition to patient populations that are likely or unlikely to respond to treatment or experience adverse side effects (Silver- Albuterol-evoked FEV 1 was higher and more rapid in Arg16 homozygotes vs. Gly16 carriers Lima et al, 1999 Arg16Gly Lower airway responsiveness to salbutamol in Gly16 vs. Arg16 homozygotes or Arg16Gly heterozygotes Kotani et al, 1999 Arg16Gly, Gln27Glu No association between genotype and desensitization to short-or long-acting  2 -agonists (formoterol vs. terbutaline) Lipworth et al, 1999a Arg16Gly Poor FEV 1 vs. albuterol concentration relationship associated with Gly16 Lima et al, 2000 Arg16Gly No association between functional antagonism of methacholine-induced bronchoconstriction with formoterol or salmeterol and genotype Lipworth et al, 2000 Arg16Gly Decline in peak expiratory flow with regular albuterol use in Arg16 vs. Gly16 homozygotes Israel et al, 2000 Arg16Gly No association between tolerance to regular salmeterol and genotype Taylor et al, 2000b Arg16Gly More frequent exacerbations during salbutamol treatment of Arg16 vs. Gly16 homozygotes or Arg16Gly heterozygotes Taylor et al, 2000a Haplotype pairs Albuterol-evoked FEV 1 improvement related to haplotype pairs (i.e., Arg19Cys (Ϫ47), Arg16Gly, Gln27Glu) Drysdale et al, 2000 FEV 1 , forced expiratory volume in 1 s.…”