PHOSPHATIDYLINOSITOL (PI), polyphosphoinositides (PPI), and other phospholipids in the phosphatidate-inositide cycle comprise only approximately 10% of total cellular phospholipids, but their turnover and chemical properties enable the inositides and related phospholipids to serve as important intracellular mediators in hormone and neurotransmitter action. Awareness of the rapidity of PI turnover dates back nearly 30 years to the pioneering work of the Hokins (1–3), who first observed this “phospholipid effect” during secretagogue action in the pancreas. During the past decade, there has been a flurry of investigative effort to further characterize and understand the biological significance of PI turnover; as a result, many hormones and neurotransmitters have been found to influence PI metabolism, new mechanisms for increasing PI turnover have been elucidated, and new insights have been developed concerning the role of PI turnover in a number of biological responses. Although the role of PI metabolism in hormone and neurotransmitter action has been the subject of several recent reviews (4–9), the present review will contrast several of the more important mechanisms that underlie changes in inositide turnover, and focus on one mechanism that has recently come to light from studies of ACTH action.