Regarding the role of aberrant autoimmunity in RGC injury, a possible pathomechanism in patients with pSS can be suggested on the basis of the results of previous studies that used the neonatal heart block model: (1) maternal anti-SSA/SSB autoantibodies cross the placenta and form IgG–apoptotic cell complexes and (2) apoptotic cardiocytes are opsonized by anti-SSA/SSB autoantibodies, which impairs clearance by normal cardiocytes [42–44]. The gene discussed is SSB; the disease is peeling skin syndrome.