The hormonal form of vitamin D may significantly influence autoimmune disease risk and severity by (i) dampening pathogenic Th17 cell IL-17 synthesis, (ii) increasing effector CD4+ T-cell sensitivity to extrinsic cell death signals, (iii) promoting CD4+CD25+FoxP3+ Treg cell and CD4+IL-10+FoxP3− Tr1 cell development and suppressive function, (iv) amplifying a Th1–Tr1 switch that may bridge two apparently stable immune states, an anti-pathogen pro-inflammatory state and a self-tolerant anti-inflammatory state. This evidence concerns the gene FOXP3 and autoimmune disease.