Well, I’m not sure if that’s really germane because I think we all agree (Behe included) that polar APOB is almost certainly involved in protecting them against hypercholesterolemia in the face of a diet high in saturated fats. I think the disagreement is in the nature of the APOB mutations - do they enhance removal of cholesterol in the blood, or do they cripple APOB-mediated loading of cholesterol into the blood (a possibility you mention above). The former would refute Behe, the latter would support him, BUT… it would require other enhancing alterations (because otherwise, the dietary fat just stays in the gut and they poop it out?). There’s no sign of those other alterations that would compensate for the diminished APOB in the list of highly selected gene variants. So this is a real stretch.
I have always maintained that it’s possible that APOB is somehow functionally diminished in polar bears, compared to brown bears. What I am saying is that there is no evidence that it is and that the available evidence argues otherwise. New evidence could change that, for sure. But the additional analysis we’ve done here in this thread and others is adding more weight on the scales. Not that this will stop the DI from trying to pretend otherwise.