The cover picture shows the binding of α-conotoxin MII to the C-loop of an α3β2 neuronal acetylcholine receptor residing in the post-synaptic phospholipid bilayer, which comprises a 3:1:1 ratio of POPC, POPA, and cholesterol. Docking studies and voltage clamp experiments show that the presence of acetylcholine in the C-loop region enhances the binding of toxin, slowing its washout. These observations indicate that α-conotoxin MII might preferentially target active synaptic clefts, which would be an evolutionary advantage. On p. 413 ff., O. M. McDougal, C. M. Maupin, et al. describe the creation of two heteropentameric α3β2 neuronal acetylcholine receptor homology models that were used in docking studies of acetylcholine, α-conotoxin, and both neurotransmitter and toxin to the various C-loop regions (i.e., α3–β2, β2–α3, and β2–β2). Subsequent voltage clamp experiments confirmed that the presence of acetylcholine enhanced the binding of toxin prolonging its effect on the ligand-gated ion channel. (Cover art designed by C.M.M.).