Researchers in the U.S. are peeling back the mystery of sunburns, investigating why the skin can become raw and fire-engine red after too much exposure to the sun.

The answer, it seems, is right underneath our skin: a common molecule called the TRPV4 gene, which, when blocked, dulls the painful effects of sunburns.

In a study published Monday in the early editor of Proceedings of the National Academy of Sciences, researchers found that when the molecule -- found in a skin's cell -- is essentially dormant or missing, the pain associated with sunburns is largely unnoticeable.

That means a potential cure for the much-hated sunburn might not be too far off.

"The results position TRPV4 as a new target for preventing and treating sunburn," said study co-author Martin Steinhoff.

He added that the results from the study could also be used to prevent and treat skin cancer.

"I could imagine (TRPV4 blockers) being mixed with traditional sunblock to provide stronger protections against UVB exposure," said Steinhoff, who is also a professor of dermatology at the University of California in San Francisco.

UVB -- or ultraviolet B -- is the most common cause of sunburns. In moderation, this component of sunlight is good for the body, injecting us with vitamin D and improving mood.

But too much of a good thing can be harmful. An overdose of UVB not only damages a skin cell's DNA, but it also increases the skin's vulnerability to cancer.

In the study, researchers used genetically engineered mice that were missing TRPV4 molecules in the epidermis, the outermost layer of the skin. Both the genetically altered rodents and a batch of normal mice had their hind paws - a part of their body which most resembles human skin - exposed to UVB.

Researchers found that the hind paws of the mutant mice didn't react to the UVB, while those of the normal mice became blistered and hypersensitive.

"We have uncovered a novel explanation for why sunburn hurts," Wolfgang Liedtke, another co-author, said. "If we understand sunburn better, we can understand pain better."

Next, researchers broke down the activities of TRPV4, tracing how UVB and the molecule interact. According to a molecular analysis, exposure to UVB stimulates TRPV4, causing a chain reaction that leads to an influx of calcium and brings forward another molecule: endothelin.

Endothelin is known to cause pain and itching in humans, which could explain why people with a nasty sunburn sometimes have an urge to scratch their skin.

To test whether the pain could be blocked, researchers applied a pharmaceutical compound called GSK205 mixed with skin disinfectant to the hind paws of the normal mice.

Similar to the genetically engineered mice, researchers observed that the rodents with the "cream" were largely resistant to the pain caused by sunburns.

Still, the researchers say caution is needed before moving forward with the study's results; they suggest further study on out how inhibition of the TRPV4 gene will affect other processes going on in the skin.