This greater transactivation capacity of the VDR in SLE patients could be causing this transcription factor to favor more polarization of the Th2 cell phenotype, which has been reported to be favored by calcitriol by inducing upregulation of GATA3 and STAT6 [12,50], and this cell profile plays a crucial role in the pathophysiology of SLE [51,52]. This evidence concerns the gene STAT6 and systemic lupus erythematosus.