Table 2 describes the relative activity of NOS and arginase with respect to the various stages of allergic asthma. In patients with severe asthma and evidence of AHR treated with corticosteroids, inhaled NOS inhibitor NG-monomethyl-L-arginine (L-NMMA) failed to potentiate bradykinin-mediated bronchoconstriction. The authors concluded that this effect reflected corticosteroid downregulation of iNOS, with reduced cNOS-derived NO leading to failure of bronchoprotection and increased AHR [48]. This evidence concerns the gene NOS3 and allergic asthma.