In summary, it is reasonable to hypothesize that obesity and vitamin D deficiency are interdependent MS risk factors, given biochemical data demonstrating vitamin D metabolite partitioning into adipose tissue and antagonism between leptin and 1,25-(OH)2D3; a window of opportunity appears to exist to lessen the MS risk in girls and reduce the accumulation of MS disability in women by resolving the dual epidemics of obesity and vitamin D deficiency. This evidence concerns the gene LEP and myeloid sarcoma.