Although scientists don't fully understand it yet, and it varies from person to person, there is a link between genetics and obesity – as you've probably figured out if you've got friends who can eat whatever they like while remaining thin.

Now new research has identified one gene that could play a role. It's called ALK (Anaplastic Lymphoma Kinase), and mutations in this gene have previously been linked to certain cancers, and identified as drivers of tumour growth.

The latest study found two particular ALK variations showing up in thin, low BMI individuals - but not in individuals of normal weight. The analysis looked at the DNA of 47,102 people aged 20 to 44 years old, taken from Estonia's 'biobank', a biological database collected from a large percentage of the Estonian population.

"We wanted to understand why," says medical geneticist Josef Penninger, from the University of British Columbia in Canada. "Most researchers study obesity and the genetics of obesity. We just turned it around and studied thinness, thereby starting a new field of research."

In follow-up tests on mice and Drosophila fruit flies, animals that had the ALK gene turned off stayed thinner than normal – even when the mice were fed what the researchers described to CNN as "a McDonald's diet".

Further tests showed that the mice without the ALK gene had lower than normal body weight and levels of body fat.

Of course correlation isn't causation. But the researchers suggest that the gene, which is highly expressed in the brain, plays a role in telling bodies how much fat to burn and how to use its energy stores.

Still, for now all we've shown is that this direct link exists in fruit flies and mice, not humans. Despite extensive research into the gene's involvement in cancer, our understanding of the ALK gene's role in human physiology remains largely unclear.

But one promising aspect of the discovery is that scientists already know how to inhibit ALK in humans because of its role in cancer development, so testing the link further is doable.

"If you think about it, it's realistic that we could shut down ALK and reduce ALK function to see if we did stay skinny," says Penninger.

"ALK inhibitors are used in cancer treatments already. It's targetable. We could possibly inhibit ALK, and we actually will try to do this in the future."

Further studies are also going to need to take a closer look at how the ALK gene operates in the brain: how it potentially balances metabolism and leads to a skinnier body shape at a molecular level.

Even if a clear link between ALK mutations and a resistance to weight gain is established, it's probably going to only be part of a much larger mix of genetic factors – as previous research has hinted at.

While the biobank data and tests on mice and flies are a good starting point at solving the mystery link between genetics and thinness, scientists are going to need a lot more data in the future before we can figure out what's really happening here.

"You learn a lot from biobanks," says Penninger. "But, like everything, it's not the ultimate answer to life, but they're the starting points and very good points for confirmation, very important links and associations to human health."

The research has been published in Cell.