Fresh frozen plasma, C1-INH protein products, the kallikrein inhibitor ecallantide, and the bradykinin 2-receptor antagonist icatibant were considered for an acute therapeutic approach, similar to hereditary angioedema attacks; however, their efficacy is not conclusive in drug-induced BK-mediated AE due to its complex pathophysiology (Figure 3) involving the metabolism of BK, BK itself, and its B2 receptors inducing vasodilation and increased vascular permeability. The gene discussed is KNG1; the disease is angioedema.