CXCL12 and Hypercholesterolemia: This myeloproliferative phenotype has been mechanistically demonstrated by our laboratory and others to be a consequence of membrane cholesterol accumulation and subsequent lipid raft formation where the common β subunit of the IL‐3/GM‐CSF receptor or CD131 becomes more highly expressed.53, 54, 55, 56 Moreover, hypercholesterolaemia promotes HSPC mobilisation by increasing plasma CXCL12 levels and disrupting the CXCL12/CXCR4 axis (Table 1).57 Activating the transcription factor, liver X receptor (LXR) prevents the myeloproliferative phenotype by activating cholesterol efflux pathways.58