Moreover, in vitro studies have shown that 1,25(OH)2D3 suppresses both TH1 and cytotoxic T cell response, whereas it enhances the differentiation of CD4+ CD25-Foxp3+ regulatory T cells, leading to significant reduction of IFN-γ and IL-17 production in many clinical conditions including TB (44–47, 113–116) (Table 1). This evidence concerns the gene CD4 and tuberculosis.