Acheson et al. (1960) observed an inverse relationship between sunlight exposure and the incidence of Multiple Sclerosis (MS). This led to the suggestion that increased levels of vitamin D caused by sunlight in some way suppresses MS. Further, super physiological doses of the metabolically active metabolite of vitamin D, i.e. 1α,25 dihydroxy vitamin D suppresses the animal model of MS i.e. experimental autoimmune encephalomyelitis (EAE). However, this response was accompanied by hypercalcemia. Hypercalcemia itself can suppress EAE. The ability of 1,25(OH)2D3 to suppress EAE in mice is largely eliminated by a low calcium diet until hypercalcemia is induced by high doses of 1,25(OH)2D3 that causes mobilization of calcium from the skeleton. Of great importance is the finding that vitamin D deficiency prevents EAE, a finding dramatically opposite to the original hypothesis. Further, vitamin D receptor knock out animals do not develop EAE supporting the idea that vitamin D does not suppress EAE. Upon revisiting the inverse relationship between light exposure and incidence of MS, a narrow band of light (300-315 nm) was discovered that prevents EAE without a change in serum levels of 25 hydroxy vitamin D (indicator of vitamin D status). Clinical trials are underway to explore the possible use of this narrow band light as a treatment to stop the progression of MS, while biochemical studies are underway to evaluate the mechanism of action of the narrow band light.