1. Nonsteroid antiinflammatory drugs inhibit prostaglandin biosynthesis in concentrations likely to be found in body fluids during therapy. The assembled evidence, together with the actions of prostaglandins, overwhelmingly supports the theory that this antienzyme effect is the mechanism of action of aspirin-like drugs. 2. Intermediates in prostaglandin biosynthesis and their nonprostaglandin derivatives such as RCS (thromboxane A2) may also play a part in the inflammatory process. 3. There is a close interplay between bradykinin and prostaglandins, not only in inflammation, but also in other systems. 4. Bradykinin stimulates phospholipase A2, thereby making available prostaglandin precursors.