 Next, we have Cynthia Turnbull from the John Curtin School of Medical Research at the Anu College of Health and Medicine, and the title of Cynthia's presentation tonight is Shining a Light on Incomplete Penitence. Diabetes, skin rashes, gut pain and diarrhea. This is what my patient Pablo lives with every day. The cause isn't a virus or a cancer, but his own body. Pablo has a severe form of autoimmunity where his immune cells attack his body. Current treatments are non-specific, suppressing the entire immune system, causing horrible side effects, and in the end, they can be ineffective. To design better treatments, my lab is looking at the genetic causes of autoimmunity. By reading the 3 billion letters of Pablo's DNA, I found a mutation which stops his T-rex cells from working. T-rex are the bounces of your immune system, and keep your drunk, overactive immune cells that could hurt your body in line. I thought this mutation could explain Pablo's disease and be a way that we could treat him, but I found something very unexpected. Pablo's mother has the same mutation as him, but miraculously, she is healthy. Her son has been sick since he was a baby, but she is fine. The strange phenomenon where mutations cause disease in some, but not everyone, is called incomplete penetrance, and it's common in many diseases, not just autoimmunity. For example, it can explain why 40% of women with BRCA mutations don't develop breast cancer, while others do. As medical scientists, it is our last hurdle in being able to accurately link the treatment of disease with genetics. I believe this protein called dectin-1 could help us overcome it. By isolating the immune cells from the blood of healthy donors, I was able to study dectin-1. When I turned dectin-1 on, it created more T-rex, recruiting more bounces to defend the body. Like the healthy donors, Pablo's mother has a working dectin-1 that protects her from her mutation. The mutation means her T-rex don't work as well, but dectin-1 makes enough of them to prevent autoimmunity. In Pablo, dectin-1 is turned off. He has fewer T-rex, which don't work well, and that is why he is so sick. If we could turn dectin-1 back on, his disease would disappear. By studying this beautiful protein, I can explain his disease and have shined a line of incomplete penetrance. We are overcoming that hurdle so that we can protect everybody from damaging mutations and prevent the diseases they cause. Thank you.