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The effect of CsA on ER glutathione was also independent of calcineurin, a prominent downstream target of the compound and a known modulator of ER Ca 2+ channels [70]

Strong arguments in favor of PS exposure being required for microvesicle release come from (1) a bleeding disorder, the Scott syndrome, where RBC neither translocate PS across the membrane nor release microvesicles (Bevers et al., 1992) and (2) the finding that a specific inhibitor of the scramblase (R5421) inhibits both PS exposure and microvesicle release to more than 50% (Gonzalez et al., 2009)