Although catalyzed by different proteins, the energy barriers for lipid bilayer fusion in exocytosis, viral fusion, and trafficking seem to be the same as those for the fusion of protein-free phospholipid membranes. To minimize this energy, fusion will proceed through a minimal number of lipid molecules, probably localized in bent non-bilayer intermediates. Experiments on phospholipid bilayer membrane fusion show the pathway of contact, hemifusion, flickering fusion pore formation, and fusion pore enlargement caused by swelling of the vesicle. Lipid curvature determines the barriers to hemifusion and fusion pore formation, while swelling-induced membrane tension drives fusion pore enlargement. Experiments on viral protein-induced cell-cell fusion and exocytosis show the same pathway with the same fundamental effects of lipid curvature and membrane tension. Thus while proteins control these reactions, lipid energetics determine the basic reaction scheme for membrane fusion.