Phospholipase A2 (PLA2) catalyzes the hydrolysis of the sn-2 fatty acyl bond of phospholipids, liberating free fatty acids and lysophospholipids (for a review see Reference 1). Its presence in pancreatic juices and in cobra venom was discovered around the beginning of the twentieth century (for a review see Reference 2). The role of these secreted PLA2s in digestion and envenomization has since been well documented. Evidence began to appear in the last several decades that PLA2s are also present in most types of cells and that they are involved in many different cellular functions including general lipid metabolism and membrane homeostasis. During this same period the view of phospholipids has also changed. What were once considered the inert building blocks of cellular membranes are now known to be important metabolic entities. Phospholipids and their metabolites are involved in a large number of important cellular control systems. This discovery has elevated PLA2s from being simple maintenance enzymes to being important players in such crucial systems as signal transduction and eicosanoid production. Through these systems, the actions of PLA2s affect a wide range of human physiological functions and diseases including asthma and allergy, the initiation and maintenance of parturition, blood clotting, atherosclerosis, sepsis, asthma, inflammatory bowel disease, and arthritis and other inflammatory diseases (for a review see Reference 3). The development of PLA2 inhibitors is being vigorously pursued. A drug that modulates PLA2 activity would have a large number of potential uses, especially as a nonsteroidal antiinflammatory agent (for a review see Reference 4). Such an inhibitor could supplement the current armament of cyclooxygenase inhibitors and new cyclooxygenase 2 inhibitors being developed to block prostaglandin biosynthesis and the multitude of approaches (for a review see Reference 5) currently being explored for the inhibition of enzymes responsible for leukotriene biosynthesis and leukotriene receptor antagonists as illustrated in Figure 1.