I think we are realising that with a lot of the sequencing activities in the last five years it’s become clear that there are too many oncogenes in many cancers, like breast, colon, lung, and there are too few oncogenes in certain kinds of cancers like ovarian, neuroblastoma. Then many of these genetic aberrations, like as in pancreatic cancer the three major genes are p53, p16 and SMAD4, all of these have lost their functions with the exception of KRAS which has gained a function. The long shot of it is that I personally feel that that kind of targeting oncogenes as a way of treating cancer has a very limited future because of many of the reasons that I just mentioned. Not to say that we have not discovered very many new oncogenes either. So that puts me in the thinking conceptually that we have done in the last thirty years to try to stop the cart, in this case the cart is the cancer cells, by targeting the horses.

The assumption, of course, the oncogenes cause cancer and if you stop them then the cart, the cancer cells, will die. I think that has worked well for HER2 positive cancer, has worked well for Gleevac, CML, it has worked for acute promyelocytic leukaemia etc. but it has now almost a sign that that has to end. That is underscored by the very few new targets that have been approved by the FDA.

So that brings me to the thinking that maybe instead of targeting the horses we have to target the cart and the cart, in my opinion, would be the transformed state of the cancer cell, irrespective of how it came to. In other words, if you were to bring someone from New York to London you can go by boat, you can go by helicopter, you can go by plane, you can go by many different ways.