Activation of CYP46A1 is protective in experimental models of Huntington's and Alzheimer's disease, where the rate of cognitive decline can be attenuated [6, 23], and its product, 24S‐HC, alongside other cholesterol metabolites, differs between MS and controls, and between relapsing and progressive MS cohorts [8, 24, 25]. This evidence concerns the gene CYP46A1 and myeloid sarcoma.