Multiple sclerosis (MS) is a long-lasting inflammatory neurodegenerative disease of the central nervous system caused by an inappropriate attack of the body' s immune system on its own cells. To date, its etiology remains highly enigmatic, with insufficient evidence on the exact cause triggering the disease. Many studies have highlighted the role of different environmental and genetic factors in its etiopathogenesis, each adding a new wedge to MS conundrum and therefore making it a multifactorial and polygenic disease. One of the entrants in the risk factor category for MS is vitamin D, and there is sufficient evidence to suggest its role in increasing the risk of MS development. MS patients have lower levels of vitamin D, and in conjunction with other factors like low sunlight intensity and genetic variations in vitamin D metabolic pathway genes, vitamin D has been adjudged as a potent risk factor for MS. The biological effects of vitamin D in the body are mediated by the vitamin D receptor that acts as a transcription factor after activation by vitamin D and subsequent heterodimerization with the retinoid-X receptor. This allows regulation of protein expression of target genes involved in diverse cellular processes including immune response and vitamin D metabolism. It clearly suggests use of vitamin D supplementation as an unconventional option for MS treatment; however, much work needs to be done to precisely determine the level and/or dosage of vitamin D required for achieving optimum therapeutic response in patients without causing adverse effects.