In old age, the liver’s DNA packaging starts to come undone. That breakdown does not change the genetic code itself. What it changes is the way the code is folded, packed, and managed inside the cell, which can decide which genes stay quiet and which ones switch on. A team at Bar-Ilan University now reports that it reversed many of those age-linked shifts in old mice by increasing levels of a protein called SIRT6. The work, published in Nature Communications, points to aging as something more dynamic than simple wear and tear. In the mouse liver, the researchers found that aging loosened chromatin, the molecular structure that organizes DNA, while pushing inflammatory genes into a more active state and weakening gene programs tied to normal metabolism. “As we age, the genome loses its proper organization,” said Prof. Haim Cohen, director of the Sagol Healthy Human Longevity Center at Bar-Ilan University’s Goodman Faculty of Life Sciences, who led the study. “Genes that should remain silent become activated, especially inflammatory genes, while genes required for normal liver …