Constitutive release of microparticles from endothelium (regulatory EMPs, beige) may be an adaptive response to cell senescence and membrane turnover (A). In contrast, binding of anti-β2GPI antibodies that mediate APS induces a procoagulant, proinflammatory phenotype (B). The study by Betaputi et al shows that anti-β2GPI antibodies activate an intracellular signal transduction pathway that leads to phosphorylation of nonmuscle (NM) myosin II and the release of potentially pathogenic EMPs (blue) that reflect these alterations in endothelial function. Release of these pathogenic or “stress” EMPs may promote thrombosis and lead to gestational and other complications of APS. It is proposed that inhibition of NM myosin II phosphorylation will attenuate stress EMP-dependent pathogenic mechanisms (C) (1), but the effect of preventing release of regulatory EMPs on cellular adaptation to stress (D) (2) requires further investigation. The authors thank Dr Rudy Fuentes (University of North Carolina-Chapel Hill) for assistance in the development of this figure.