While M2 macrophages can exhibit anti-inflammatory effects through phagocytose apoptotic cells, a process called efferocytosis, PR3 inhibits this process (63), leading to incomplete neutrophil clearance and pro-inflammatory M1 macrophage involvement (64), which participate in GPA granuloma formation together with M2 macrophages (65). This evidence concerns the gene PRTN3 and granulomatosis with polyangiitis.