FTM, based on what I understand about the mechanism that exposes PS, it would be expected that PS is exposed when necrosis is present. Similarly, the methodology where a coated or enveloped virus enters a cell, replicates and the virions coat themselves with cell matter would be statistically structured to expose inside out PS from damaged cells. Otherwise, the virus would have to take on the duty of picking up PS and orienting it so that there was no external exposure.
One of the benefits of Bavi is that it would adhere indiscriminately to exposed PS and exposed PS is intrinsic to tumor necrosis or viral envelope formation.
I don't see a mechanism whereby cell genetics could cause for spontaneous alignment so that no PS is exposed or that would have exposed PS not available for getting attached to Bavi. What you appear to be suggesting is that there are genetic or other differences such that a prescreen might be done to screen out patients that don't incur exposed PS through necrosis or the enveloped virus replication process. For Bavi and exposed PS, I don't think that can happen.
Am I missing something here?
Best wishes and IMO.
KT
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