Why wasn't a group like that, like us, which was well supported, well resourced by ICRF, able to participate more in the great developments which were taking place in immunology world-wide? And I think, in a nutshell, we were slow to do two things. One of them was to take the immune system apart and do it all in vitro, and the other was to contribute to- which we did not do- to the molecular understanding of the immune system, how the immunoglobulin genes worked, how, more importantly, because we were really T-cell people, how the T-cell receptor worked, how MHC molecules presented antigens to T-cells. Those were all great developments. Restriction, and the essential need to- for T-cells to recognise the MHC molecules as well as the peptide, for which a Nobel Prize was given during that time, we were kind of left out there. I have asked myself why we weren't more successful. As far as the- the in vitro work is concerned, that developed in a way- things- projects have a life of their own in a research group- and it developed in really an unfortunate way. Mark Feldman, just as we were coming to University College, Mark Feldman came from- he was a student of Gus Nossal in Australia, and Gus sent him to me to join the group, and Mark Feldman was a pretty impressive scientist, he set to work very hard. And he set up- of course he'd been- in Melbourne, he had got all the in vitro stuff working- he set up all that at University College, he organised us to get the hoods which were needed and so on and so forth, the reagents, but his research took a somewhat unexpected direction. He became interested in, perhaps I should say obsessed by, immune suppression, the regulatory part of the immune system which prevents reactions, prevents auto immunity, which makes- drives the immune system to make responses to viruses or bacteria in an appropriate way. And what went wrong with Mark's research I really don't know but over, I think it must have been well over ten years, he worked on suppression and on factors which he thought were mediating suppression, and it kind of all blew over. He wasn't the- it wasn't- it wasn't the only place in the world which was working on that, Benacerraf who I mentioned earlier, his group in America developed the same focus and I suspect that there was a bit of- bit of- each group was leading the other up the garden path. The experiments weren't done as critically as they should have been done. Certainly, as leader of the group I bear responsibility for that, some responsibility for that, and Mark eventually left the the tumour immunology group and moved over to rheumatology in the Kennedy Institute in London, where he made this fabulously important contribution that I have already mentioned, of developing anti TNF therapy. The suppressor factors and suppressor activity is still a murky area but nobody still knows whether there was not some truth somewhere in that but where it was I don't know. I became also interested in suppression. I was not- I didn't think it was right that a group of our size should- should stand apart from those important developments in T-cells and became interested in a different aspect from what Mark was doing and that was in the way certain MHC molecules seem to encourage the development of suppressive activity, and you could- we, I would say sort of developed, perhaps perfected I hope, a particular kind of experiment where you combine a suppressive MHC molecule with a non-suppressive MHC molecule or rather a suppressive gene and all the molecules which it encodes, with an activated gene and all the molecules which it encodes scattered around the immune system. And the suppressive one can win, it can turn off the activity of the active one, and there is no doubt about that as a scientific finding, that has been found again and again. But I- it was not until later, when I left to go to Berlin, that I got anywhere near the root of the mechanism involved there, and I think I did eventually.