Then, we found that IgE, especially autoreactive IgE, mediated basophil activation in SLE, based on the detection of abundant total IgE, autoreactive IgE, and the higher expression of the high-affinity receptor for IgE (FcεRIα) on basophils in patients with SLE, and in vitro experiments including isolated basophils cocultured with the serum of patients with SLE and PEG precipitation CIC (containing IgE). This evidence concerns the gene FCER1A and systemic lupus erythematosus.