Thus, while the induction of protein citrullination, the exposure of PR3 and MPO, and the extrusion of chromatin during NETosis are attractive elements (but not exclusive for NETosis) for diseases like RA, ANCA-associated vasculitis, and SLE, respectively, features like the targeting of Ro and La and their association with photosensitivity in SLE can be more easily explained by ultraviolet-B (UVB)-induced keratinocyte apoptosis (Casciola-Rosen et al., 1994) than by NETosis. The gene discussed is PRTN3; the disease is systemic lupus erythematosus.