In Apoe–/– and Ldlr–/– mice, hypercholesterolemia results in an expansion of monocyte progenitors and systemic monocytosis (Soehnlein et al., 2013; Rahman et al., 2017), likely by a modulation of reverse cholesterol transport in Hematopoietic Stem Progenitor Cells (HSPCs) (Yvan-Charvet et al., 2010; Murphy et al., 2011) and accelerated extramedullary hematopoiesis (Robbins et al., 2012). The gene discussed is APOE; the disease is familial hypercholesterolemia.