It is acknowledged that in APS the dominant population of pathogenic autoantibodies target the circulating autoantigen β2GPI.26, 27, 28, 29 To demonstrate if this APS IgG-mediated pathogenicity of cardiomyocyte H/R injury was mediated through β2GPI autoantibodies, cells were cultured in media containing β2GPI-deficient human serum in the presence of IgG from the different groups studied. This evidence concerns the gene APOH and autoimmune polyendocrinopathy.