The finding that increased ADA activity in tuberculous pleurisy is due largely to increased activity of the ADA isoenzyme ADA-2, together with the fact that the only cells in which ADA-2 has been found are monocytes/macrophages, led Gakiset al. to attribute increased ADA activity in pleural TB to the stimulation of monocytes/macrophages by live phagocytosed micro-organisms [16]. Here, ADA2 is linked to pleural tuberculosis.