Calcitriol enhances the polarization to the Th2 phenotype [11], and the contributions of Th2 cytokines to the renal disease include the production of IL-6 and IL-4 by activated basophils that leads to autoantibody deposition in the kidney via enhanced Th2 response and B cell activation, promoting the release of Th2 cytokines such as IL-10, IL-13, and IL-6; the influx of inflammatory cells; and renal manifestation in active SLE or SLE patients with LN, compared to patients without renal disorders [4, 5]. This evidence concerns the gene IL10 and kidney disorder.