A recent piece of research indicated that neutrophils from SLE patients release neutrophil extracellular traps (NETs) complexed with IL-33 in the blood and other inflamed tissues, such as kidneys and skin, and contribute to the production of type I IFNs through interactions with the ST2L receptor on plasmacytoid dendritic cells (pDCs) [40], implying that IL-33 and its receptor ST2 may contribute to the pathogenesis of autoimmune diseases, especially in patients with SLE. The gene discussed is IL33; the disease is autoimmune disease.