Here is a great example, from the irreplacable Carl Zimmer, of how the theory of evolution helps to guide new research that may provide enormous benefit to us in understanding and combatting diseases that are based in genetic causes. Since I can’t possibly express it any better than Zimmer, I’ll let him do it:
Claes Wahlestedt, one of the scientists who will be setting up shop on Scripp’s Florida campus, searches for new drugs by understanding how the human genome evolved. Genes only become active in our cells when certain proteins lock onto small stretches of DNA near them called enhancers. The enhancer bends until it meets up with another piece of DNA called a promoter. That bending acts like a switch, turning on the gene, allowing it to produce a protein. The elements of these switches are very hard to pinpoint in the human genome. That’s because they are very short and are located hundreds or thousands of positions away from the gene they control. Making matters worse, they are usually nestled within long stretches of DNA that don’t appear to serve any function. Finding these switch elements could prove very important to medicine. A mutation to a switch may make people prone to certain diseases or respond poorly to certain medicines.
Wahlestedt is finding these promoters, and it’s evolution he’s using as his guide. He and his colleagues described their approach in an open-access paper published earlier this year in the journal BMC Genomics. They lined up the sequences of human genes with their corresponding genes in mice. They then looked near the genes, in the long sequence of non-coding DNA, searching for short stretches of DNA that were similar in both species. Their reasoning was this: if a piece of non-coding DNA in the common ancestor of humans and mice didn’t serve an important function, it might pick up mutations over time without causing any harm. As a result, most non-coding sequences should be noticeably different in humans and mice, because we share an ancestor that lived some 100 million years ago. But switches probably played a vital role in that common ancestor, and most mutations that struck them would have had a devastating effect. Natural selection should have prevented most of these mutations from becoming fixed in both humans and mice. As a result, parts of DNA involved in switching genes on and off should look very similar in humans and mice, unlike the other non-coding DNA.
Now, here’s the likely response from creationists to this: “You don’t need evolution to account for this because it’s possible that God just used the same switches over and over again as he created new species.” But this actually demonstrates why evolution is such a powerful theory and creationism is just an ad hoc explanation, because there is one big difference between these two predictions: in the case of evolution, this prediction must be correct if common ancestry is true, whereas with creationism the opposite could be true and they would still count it as evidence for their “theory”. If the switches in humans turned out to be in totally different places, or using entirely different gene sequences, than in mice, the creationists would simply say, “See, that proves that evolution is false, but creationism can account for that easily – obviously, God created a new switch from scratch.” So this is a perfect example of why creationism (in any form), because it can account for any possible set of data, even completely opposite sets of data, is not a genuine scientific theory. If it can explain any possible reality, it can’t be tested because no potential evidence could possibly show it to be false.