The clearest evidence for a role of excessive myelopoiesis in neutrophilia and monocytosis comes from studies of animal models with hypercholesterolemia and genetic deficiency in genes involved in cholesterol efflux from hematopoietic cells such as Abca1−/−/Abcg1−/− or Apoe−/− mice [5, 6]. Here, APOE is linked to familial hypercholesterolemia.