ASPIRIN prevents prostaglandin (PG) generation by directly inhibiting the cyclo-oxygenase enzyme responsible for PG biosynthesis^1–3. In addition, there is now conclusive evidence that anti-inflammatory steroids can also prevent PG generation^4–13. Unlike the aspirin-like drugs, steroids have no anti-cyclo-oxygenase activity but exert their action by preventing the release from phospholipids of the fatty acid substrates required for PG biosynthesis^4–9,12,13. We have shown that stimulation of thromboxane A₂ (TXA₂) release by agents such as histamine, 5-hydroxytryptamine and rabbit aorta contracting substance-releasing factor (RCS–RF) (but not arachidonic acid) is inhibited by anti-inflammatory steroids, and that their potency in this action closely parallels their anti-inflammatory activity^12,13. Furthermore, their mechanism of action involves the inhibition of phospholipase A₂ activity, and thus of arachidonate release within the lung^12,13. In several other tissues, the mechanism of steroid hormone action depends on the combination of thesteroid with a cytosolic receptor protein, the translocation of this drug–receptor complex to the nucleus and the initiation of protein biosynthesis^14–16. We now show that similar events occur in the guinea pig perfused lung before inhibition by steroids of phospholipase A₂ activity (and thus TXA₂ generation). We have discovered a steroid-induced factor which mimics the anti-phospholipase effects of these anti-inflammatory agents.