In addition to MPO and PR3, ANCAs have the potential to target various other neutrophil-derived molecules, including α-enolase, azurocidin, bactericidal permeability-increasing protein (BPI), cathepsin G, elastase, defensin, lactoferrin, lysosome-associated membrane glycoprotein 2 (LAMP2), and moesin; however, these ‘minor’ ANCAs generally exhibit low pathogenicity and are not typically associated with vasculitis [78]. The gene discussed is PRTN3; the disease is vasculitis.