In support of this concept, increased primary granule degranulation by AATD neutrophils in response to leukotriene B4 and BLT1 membrane receptor engagement has been demonstrated [25], and was further confirmed in a recent plasma membrane proteomics study, demonstrating increased activation of the Rho GTPase Rac2 and extracellular MPO release [29]. The gene discussed is LTB4R; the disease is alpha 1-antitrypsin deficiency.