Yes, I mean, I think it actually is quite remarkable and the mechanism is really quite beautiful. As you might expect, it's tied to the VTA or the central tegmental area and the nucleus secumbants. If you look at the preclinical data again these are animal data, but what you see is reduction in cravings or so reduction in self administration, reduction in relapse, both Q induced relapse and stress. You see extinction. You see all of these across cocaine, nicotine, alcohol, opioids and interestingly across binge eating, I mean the binge eating paradigm with true binge eating not just appetite suppression. And you mentioned sort of this common this is there some sort of common thread. Well, the operating theory I think I mean certainly NIDA and the leaders of NIDA believe that it's dopamine driven, right. And when you look at the mechanism of PDE7, what PDE7 inhibitors then appear to do is in the acute addiction, where patients are hyperdopaminergic, high levels of dopamine, they bring those dopamine levels back to normal, making the patient affectively udopaminergic. In the setting of chronic addiction, where patients are - and addicts are really hypodopaminergic through the nucleus secumbants what we're seeing is what appears to be happening is an increase in dopamine levels, again returning the patient to - or the addict to a udopaminergic level. The importance of all of this too is that it's done -- it appears without affecting the reward system. And that's really the one of the most interesting components of this, right, because all of these other anti-addiction agents decrease the craving to some extent, but it also have an effect on the reward system. So, you may decrease the craving to some extent for the drug, but you also reduce the patient's enjoyment of food, socialization, sex, sports whatever. That makes it kind of tough, with respect to compliance. But if you can do all of the things that we're talking about without affecting the reward system, so you're really just reducing the craving, it would be, truly something quite remarkable and really unprecedented. Those preclinical data need to hold up in the clinic to really deliver on that promise. But obviously, we're excited about the data, the consistency of the data, the reproducibility across multiple drugs of addiction, across multiple models, yes, we're very excited about it, and we think it could be a very important drug. As we said, addiction $0.5 trillion a year, it's bigger than cancer and diabetes combined, you know.