Our group has proposed a similar “hapten-carrier” model to address the breadth of the autoantibody response in SLE, in which an apoptotic or other dying cell—in particular, its non-protein determinants (e.g., phospholipid or DNA)—serve as “haptens,” while β2GPI serves as the “carrier protein” and promotes the activation of β2GPI-reactive T cells (16). Here, APOH is linked to systemic lupus erythematosus.