Alternatively to its pro-apoptotic role in COPD, PR3 may paradoxically prevent apoptosis in granulomatosis with polyangiitis (GPA) by associating with calreticulin, through co-externalisation with phosphatidylserine by phospholipid flip-flop via phospholipid scramblase 1 (PLSCR1), to override the ‘eat me’ signalling [112]. Here, PRTN3 is linked to chronic obstructive pulmonary disease.