 So what we found is a new way that cancer cells can hijack our white blood cells. These cells that normally protect us to help them spread to other tissues. And that is related to this image here, which is something called electron microscopy, where you can see very high detail. So this white blood cell that we have looked at is called a neutrophil. A neutrophil, the very common in our body, is our most common white blood cell. It's normally working by attacking the bacteria or the yeast, literally eating them inside the cell. But some of these microorganisms have developed ways to avoid being eaten. And then the neutrophil has countered again with these very peculiar methods that sort of indicate in this picture. So up here you have a normal neutrophil. It's nice, smooth and round. And down here is a neutrophil that has taken its DNA, the DNA that's normally inside the cell and is encoding for all our building blocks in our body. This DNA is instead by the neutrophil being used sort of like a spiderweb. And in that spiderweb it's put in the enzymes and toxins that are normally used to kill the bacteria inside the cell. But now instead it kills the bacteria outside the cell in tangling them in the spiderweb and then killing them in place. So we were looking at how cancer cells are arriving to the new tissue. So when cancer cells spread from the original tumor to different tissue they often spread through the blood. And the spiderweb we think are helping the cancer cells spread because these enzymes that are normally used to kill the bacteria also can digest and dissolve our tissues. So by doing so there's more holes and the cancer cells can better get into the tissue and better expand. So the big question for us now is can you prevent metastasis by targeting this process by preventing the whiteboard cells from forming nets or by other way attacking these spiderwebs? And here was a clue that in cystic fibrosis these neutrophils are forming spiderwebs at quite high number because of the persistent infections that are in the lungs. So you can treat cystic fibrosis patients with an agent that dissolves these spiderwebs. And that agent we tried to test it in the mice to see if it worked. The problem we had though was that once you put it inside a body now you're just not just inhaling it but you're putting it in the blood. It has to go where the cancer cells goes. Now our body starts eliminating this agent. So we were collaborating with a group at Dana Faber, Michael Goldbeck's group and they have developed something called a nanoparticle that when you attach it to this dissolving agent called DNAs now you have a drug that is stable in the body for much, much longer. So in the experiments we are doing in the lab right now we are trying to find out what is the best way forward? How do we identify the patients that could benefit from this kind of treatment? And how do we best attack these spiderwebs? Are there alternative ways of attacking it? When should we attack it? All these kinds of logistic problems that are critical to address before you start giving this type of treatment to patients.