In uveal melanoma, VDAC1 helps keep the tumour's genome stable — silencing it kills cells and unleashes DNA damage

Over in Yichang, China, Rongrong Wei and Liyuan Gao went hunting through data on uveal melanoma (the most common eye cancer in adults) for genes tied to "R-loops" — those messy little DNA–RNA tangles that can wreck a genome. VDAC1, of all things, popped out near the top.

When they switched it off in tumour cells, the cells slowed down, stopped migrating, and started dying — but their DNA also got more tangled and damaged. So here VDAC1 isn't just the metabolism-and-death channel we usually talk about; it seems to help tumour cells keep their genome tidy enough to keep growing. New angle on an old protein, and a reminder that VDAC1 wears a lot of hats.