Although anti-RPA described in the present study recognizes the unphosphorylated form of RPA32, in contrast with the preferential recognition of the phosphorylated form of RNAP II by certain SLE sera [33], it is tempting to speculate that abnormal phosphorylation, disassembly of RPA, and degradation triggered by ultraviolet or chemicals are associated with the initiation of an autoimmune response to RPA. The gene discussed is RPA1; the disease is systemic lupus erythematosus.