This probably results from a failure to generate cholesterol-derived oxysterols required to activate LXR, similar to what occurs in Niemann–Pick disease type C fibroblasts30, which are unable to export cholesterol from lysosomes and, consequently, have deficient upregulation of ABCA1 and cholesterol efflux to apoA-I32. This evidence concerns the gene ABCA1 and Niemann-Pick disease type A.