The drug lowered the levels of two proteins in the arteries that are known to break down plaque structure, which might help keep plaques from bursting.

Mice treated with the drug had much smaller dead-cell areas in their artery plaques—almost half as big—which might mean their plaques are less likely to break open.

The drug didn’t lower the mice’s overall cholesterol, so its benefits must come from something else—like reducing inflammation or cell death in plaques.

The drug lowered two key inflammation signals in the blood by nearly half, which may help calm down the body’s harmful immune response in the arteries.

The drug didn’t affect blood sugar or fat levels in the blood, so its benefits aren’t due to improving how the body handles sugar or fat.

The mice didn’t gain or lose weight or eat differently with the drug, so the benefits aren’t just because they were eating less or changing their metabolism.