When cells are starved of essential nutrients, autophagy, a process of self-digestion, is induced for cell survival. Previous studies in mammalian cells have shown that a structurally intact Golgi complex negatively regulates the induction of autophagy. Other studies from the Brown lab have shown that the architectural integrity of the Golgi complex requires the activity of cytoplasmic Phospholipase A2 (PLA2) enzymes. For example, inhibitors of PLA2 enzymes cause the intact Golgi complex to fragment into “mini-stacks.” To further investigate the relationship between autophagy induction and Golgi architecture, HeLa cells were treated with the PLA2 inhibitor ONO-RS-082 (ONO) to disrupt the Golgi, and its effect on autophagy was visualized by imaging the association of the autophagosome marker protein LC3. Normally, LC3-labeled nascent autophagosomes are evenly dispersed throughout the cytoplasm; however, I found that treatment with ONO caused autophagosomes to cluster in the center of the cell. This clustering occurred in both a time- and concentration-dependent manner. This result reveals a previously unknown connection between autophagy and the Golgi complex.