Venki Ramakrishnan: Everybody knew that the ribosome is a target for lots of antibiotics, and it’s because it’s such an ancient molecule that our ribosomes are somewhat different from the ribosomes of bacteria. So some compounds will bind better to the bacterial ribosome and stop them from working, and they won’t do much to our own ribosomes. That’s how these antibiotics work. There are many of them: tetracycline or erythromycin, azithromycin. All of us, at some point, need them. We all knew that, and we knew that once we solved the structure, we’d be able to figure out exactly how these antibiotics bound to the ribosome. If we knew that, we could design compounds that bound even better at these sites or even to new sites. So that was not unexpected. In fact, when we published the first structure of this — what I call the small subunit — there were two back‑to‑back papers that we published. One was just a structure. Another was a structure with three antibiotics bound to it, to show how they stop different aspects of ribosome function. Not surprisingly, pharmaceutical companies have taken this up.