Researchers discover molecular trigger of inflammatory bowel disease

Interesting. Underscores why TNF-blockers work. Ultimately tough if they can target (reverse the epigenetic change of this gene that fails to naturally suppress TNF) further upstream that should be good.

Even better than reversing the epigenetic change would be preventing it in susceptible individuals.

The research also suggests that change in gut microbes may be more consequence than cause of UC. This would set some limits on whether probiotic therapies (including FMT) could ever be curative.

"When they raised the zebrafish mutants in a germ-free environment, TNF was still activated, though to a lesser extent. The results suggested that losing uhrf1's brakes was enough to head TNF on a course for destruction, even without that extra push from intestinal microbes."

Targeting something to be more active is usually tougher than turning it off. Moreover, uhrf1 is probably regulating numerous other genes so modulating its activity could have many side effects. They need to go further up the chain still to figure out the cause.