The research was headed by Dr James Lee of the genetic mechanisms of disease laboratory at the Francis Crick Institute in London, with the findings published in the science journal Nature.

Dr Lee said the team “stumbled” upon the discovery, while looking at a “gene desert”; a part of DNA on chromosome 21 that does not code for proteins.

This section of DNA has previously been linked to autoimmune diseases such as IBD.

The researchers described how they found this section of DNA acted like a volume control for nearby genes.

The risk of IBD was increased when the “enhancer” was only found in immune cells called macrophages, and boosted a particular gene called ETS2.

“What we have found is one of the very central pathways that goes wrong when people get inflammatory bowel disease and this has been something of a holy grail,” Dr Lee said, according to The Guardian.

“Even for pure, fundamental immunology this is a really exciting discovery. But to show this is dysregulated in people who get disease not only gives us a better understanding of the disease, it tells us this is something we can treat.”

Scientists believe that a class of anticancer drugs called MEK inhibitors would dampen the gene’s activities, and reduce gut inflammation.

It is believed that 7 million people worldwide are affected by IBD, particularly the two main forms in Crohn’s disease and ulcerative colitis.