The SIRT1 protein begins to neglect its role as a gene suppressor (which normally prevents genes from being expressed in the wrong body tissues — a process thought to contribute to some diseases) in mice whose DNA is damaged, and this may contribute to aging, Harvard Medical School researchers have found.

This raises the hope that, if gene-suppressing proteins become similarly overworked in humans, they could become prime targets for drugs to keep us young.

This possibility is boosted by the team’s finding that mice engineered to over-express the gene for SIRT1 were better at repairing DNA, more resistant to cancer, and maintained a more youthful pattern of gene expression.