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"...ion handling..." A potential channelopathy reference again? Are we talking channelopathies as downstream effects, and abnormal RBC deformability simply further downstream? I know - way too speculative. Also, I always thought of channelopathies as the starting point, ie, genetic, usually...

Our's would be an acquired altered RBC deformability, if applicable - I think (it could be genetic, but adult onset in some and childhood onset in others makes that proposition seem less likely). This paper addresses hereditary hemolytic anemia. What about acquired hemolytic anemia, or...

This paper specifies skeletal muscle. Maybe the Australians were on to something with the calcium channelopathy theory. But the tie to EV escapes me. Are EVs remnants or blebs from skeletal muscle cells?

Not unlike the logic underpinning MS, truth be told.