This finding, in a population where there is no influence of antiretrovirals on the CD4 level, could be explained by the role played by the vitamin D/vitamin D receptor system in activation and TCR signaling in naive T cells [16], and fits well with data showing that vitamin D deficiency is associated with clinical progression of untreated [17] or treated [18], [19] HIV disease, including AIDS-defining events [18], and with a poorer CD4 restoration on treatment [20], [21]. The gene discussed is VDR; the disease is vitamin D deficiency.