I am going to give you an overview and an introduction to the caspases, their structure, the substrate binding cleft, inhibitor interactions and cellular interactions. I think from listening to Seamus earlier on, that my talk is reasonably complementary, and not overlapping, which is good! Then I will talk about our work on caspase messenger RNA expression, caspase inhibition and production of inhibitors and what their biological actions are. And finally, since this is the Society for Medicines Research, I thought I should also share with you some practical issues about this whole area which I think are very germane. A property of caspases that is especially interesting in terms of neuroprotection and neurodegeneration, is that they are constitutively expressed as latent enzymes, so that in neurodegenerative diseases they are activated. That means there is potential for a drug which targets these enzymes to have reduced side effects. That is very important when you consider that in diseases like stroke, where drugs have been developed to inhibit NMDA receptors, and ion channels, that none of them have succeeded in clinical trials either because they lack efficacy in human studies, or they have side effects. All of those channels, or receptors, are constitutively active, and therefore there is the likelihood of side effects during treatment; the point is that the latency of caspases in tissues that are not involved in neurodegeneration means they are potentially not a target.