 Cardiovascular disease is killing us. It's the leading cause of death in the Western world and that includes right here in Australia. If you were to go up to Stirling Highway and take a look at the UWA clock tower, every time that minute hand moves 12 minutes, one Australian dies from cardiovascular disease. Genetic mutations to contractile proteins in the heart contribute to this burden. Contractile proteins are important in the heart because they allow it to expand and contract and therefore maintain the heartbeat. Mutations to these proteins mean that the heart can no longer beat properly and this leads to the development of an enlarged heart. Strikingly, 1 in 200 of the general population have these mutations, with the outcome being the development of sudden cardiac death. Sadly, this is the leading cause of death in the young, including in children and young healthy athletes. Next I'll show you a video of a young healthy athlete with one of these gene mutations. While on the soccer field, this young man collapses. He's having a cardiac arrest. Fortunately, due to a defibrillator that's implanted in his chest, he's immediately administered a shock that kick-starts his heart back into rhythm and he survives. However, this is not the case for most people with these mutations. Most people with these mutations don't actually know they have the mutation until they collapse with cardiac arrest and the outcome is fatal. So, how do these gene mutations result in sudden cardiac death? What is the missing link? Well, using technology where we can assess the function of individual heart cells on a microscopic level, we find that heart cells from healthy hearts contain a channel in their cell membrane. This channel is important because it initiates the heartbeat, much like the starter motor in a car. They're directly collected to these scaffolding proteins and these scaffolding proteins are directly connected to mitochondria. And in the heart, mitochondria are the powerhouses of the cell and they are responsible for producing the energy required to maintain the heartbeat. So, the channel and mitochondria communicate with each other to maintain a normal beating heart. In cells from enlarged hearts, these scaffolding proteins are severely disrupted. This results in a communication breakdown between the channel and mitochondria, resulting in an overproduction of energy. With this, the heart works harder and since the heart is a muscle with increased work, it gets bigger to the point where it can no longer function and it fails. So, how can we prevent this from happening? Well, with support from people like you, we're the first group in the world to design peptide therapy that targets this channel. This peptide therapy restores the communication between the channel and mitochondria and normalises energy production. This prevents the heart from working too hard, reduces the stress on the heart and prevents it from getting too big and failing. Currently, with our clinical collaborators in Sydney, we are on track to translating this therapy to the clinical setting to decrease the devastating impact of this silent killer. Thank you.