One other thing, Jon I just wanted to mention that build on, what Marianne was saying, I think one of the things that we always try to remind folks, we think that 1002 is well differentiated from for example the PCSK9s that are in development because we keep saying to it's an oral therapy and the tradition of all of the successful LDL cholesterol lowering therapies in the history of the world, that's one point of emphasis. I think secondly that, we lower both LDL cholesterol and hsCRP and then finally, that in a payer constraint, what we are seeing is an increasingly economically payer constraint environment that relatively lower cost, small molecules we think will always have a place in the treatment armamentarium for physicians and then from a regulatory standpoint, we always folks on the team have been around long enough to remember that, the LDL hypothesis that lowering LDL cholesterol leads to lowering the cardiovascular disease risk is not just the been the statin's but there have been other therapeutic alternatives that have provided that same lower LDL cholesterol. We also get a reduction in cardiovascular disease risk and so we like to remind folks that we are, in statin tolerant patients by definition not catch thing the same hypothesis that IMPROVE-IT is, which on top of statin or the some of the other recent trials, whether it's AIM-HIGH or HPS2-THRIVE. All of which were testing a different hypothesis than the one that we are testing in, statin intolerant patients which is, primary LDL lowering and a patient population that has a very high level of unmet medical need is demonstrated by the very high baseline LDL levels, you have seen not only in our trial, but in the trials the other statin intolerant trials that have been in this therapeutic area. So we try to differentiate that the hypothesis that we are testing is different than perhaps what the PCSK9 sponsors are doing or any of the recent trials have done, which is always been testing this hypothesis of incremental LDL cholesterol lowering on top of statin, that's clearly not our focus with statin intolerance.
Jonathan Eckard – Citi: Perfect and then one question, is that some of the other again the PCSK9s and the design of their statin intolerance trials. It seems like, in a definition of statin intolerance, they have been doing a little bit of back pedaling with regards, what they initially did versus the FDA's definition of statin intolerance. I was wondering, could you outline a little bit of the nuances of your trial design statin intolerance because you guys have both statin tolerant and intolerant patients. Could you maybe articulate some of the potential benefits of including both those populations and how the findings from this trial could provide you a little bit more insight and maybe somehow, how the other statin intolerant trials have been designed?