An increased level of TF-bearing microparticles in PNH patients, decreasing after eculizumab therapy, was previously described but this was not correlated to changes in TF microparticle activity or total microparticle factor Xa generation.[7] In our study, the addition of anti-TF antibodies did not affect thrombin generation results more significantly in PNH patients than in control subjects, reinforcing the assumption that most of the TF on the circulating EVs in PNH patients is encrypted and nonfunctional.[7]. The gene discussed is F10; the disease is paroxysmal nocturnal hemoglobinuria.