The overall picture we have now is that glutamine expansion causes some aspects of the pathology of SCA1 in part by enhancing the activity of the domain that is outside the glutamine repeat.

We had known that the expansion of the glutamine tract within Ataxin-1 probably interfered with normal clearance of Ataxin-1, meaning that it accumulated in cells.

We had been accumulating clues that the glutamine tract expansion is clearly what is important for disease because that's the mutation. But we also concluded that there was something else beyond the glutamine that's really mediating the toxicity of the protein.

Importantly, such insights can now guide studies that focus on the normal function and interactions of these proteins and how they might be enhanced by disease-causing mutations. These studies could give better understanding of how the proteins cause disease.

I do not deny that there may be other well-founded causes for the hatred which various classes feel toward politicians, but the main one seems to me that politicians are symbols of the fact that every class must take every other class into account.

It's still a required class -- it's not like it's going to be super-fun -- but at least you're getting stuff out of the way quicker, and getting prepared.