Researchers discover how to turn one germ's drug resistance into an Achilles' heel

Decades of reliance on the antibiotic rifampicin have fueled the rise of drug-resistant Mycobacterium tuberculosis (Mtb). But as the bacterium mutates to protect itself from the drug, it also creates new weak points that other therapies could exploit. Now, a new study published in Nature Microbiology shows that the most common rifampicin-resistance mutation slows bacterial RNA polymerase, creating vulnerabilities that future combination therapies may be able to target.