Overall, we propose a-multi-step-mechanism for the formation of auto-antibodies in SLE and in Lupus nephritis in which auto-antigens are post-translationally modified and exposed to the environment in NETs where they are recognized and exposed to B cells by specialized TLRs that drive the isotype switching from the common IgG3 to IgG2 that is typical of SLE. The gene discussed is IGHG3; the disease is lupus nephritis.