Stay on target. That’s the mantra you hear in labs and biotech companies around the world as they snip away at DNA. All the techniques for gene editing—from the famous Crispr-Cas9 to the older TALENs and zinc-finger nucleases—share a problem: Sometimes they don’t work.

Which is to say, they have “off-target effects,” changing a gene you don’t want changed or failing to change a gene that you do. And DNA is not something you want poorly rewired. That goes double if you’re trying to make money; companies working on genome-editing based products are valued in the billions of dollars. That’s why two scientific articles published today in the journals Nature and Science are so important—they tune genome editing up.

The Nature paper chases precision at a literally basic level—the bases, the As, Gs, Cs, and Ts that are the individual units in the genetic code. Crispr-Cas9 works by slicing through the two strands of bases that spiral to create DNA’s famous double-helix. But another approach, single base editing, actually converts one base into another—since the bases pair in predictable ways, A to T and G to C, that modification flips a single genetic “bit.” Until now, scientists have only been able to change a G-C base pair into an A-T base pair.

The new paper takes the other angle, describing an editor that changes adenine—the “A”—into a base called inosine, which the cell’s protein-building machinery reads as guanine, the “G.” When that molecular machine puts a little nick in the complementary strand of DNA across the gap where the T is, the cell’s DNA repair machinery “fixes” it by slotting in a C. In other words, it’s an A-T to G-C base edit.

How cool is that? “This class of mutation, changing a G-C to an A-T, accounts for about half of the 32,000 known pathogenic point mutations in humans,” says David Liu, the Harvard chemist whose lab did the work. Liu’s lab has already used this editor to fix—in cell cultures—the mutation that causes hereditary hemochromatosis, which causes a person to retain too much iron, and to treat sickle-cell anemia.

Getting there wasn’t easy. In biology, changing one molecule into another is usually the job of a natural nanotechnological marvel called an enzyme. Enzymes that turn adenine into inosine are called adenine deaminases, but none exists that’ll transmogrify adenine embedded in a strand of DNA. So Liu’s team built one, putting engineered bacteria under evolutionary pressure until it built an enzyme that would target A’s in DNA.

And it goes to the right A, too. One of Crispr’s components is a molecule of “guide RNA,” a length of genetic stuff that points to a target like the scrap of clothing you hand a bloodhound before a hunt. Liu’s editor uses that part. “Normally Crispr-Cas9 makes a double-stranded cut in the DNA,” Liu says. “We used a form of Crispr-Cas9 that’s crippled. It cannot cut the DNA.” But it still stays on target.

The research in the Science paper takes a different tack on A-to-G conversion. This one, from the lab of Broad Institute researcher Feng Zhang, incorporates an adenosine deaminase (a molecular cousin of the adenine deaminase in the Liu paper) into Crispr-Cas13, a variant genome editor that works on RNA—the copy of DNA that cellular machinery reads to build proteins. Zhang’s team calls it “RNA Editing for Programmable A to I Replacement,” or Repair, proving that if the fights over Crispr’s genesis and patent have taught researchers anything, it’s to come up with better names.