In conclusion, since C1-INH inhibits the proinflammatory effect of sPLA2, the data collected in this paper suggest that patients with angioedema with C1-INH deficiency could have a greater and uncontrolled inflammatory response to endogenous (human) and exogenous (bee and snake venom, etc.)sPLA2s compared to healthy subjects. The gene discussed is PLA2G2A; the disease is angioedema.