An increase in the number of Ly6Clow monocytes under hyperlipidaemic and atherosclerotic conditions partially depended on CCR5, and depleting the number of patrolling Ly6Clow monocytes via knockout of transcription factor Nr4a1 (Nur77) determined the survival or death of Ly6Clow monocytes in ApoE/− mice, resulting in pronounced endothelial apoptosis and exacerbated atherosclerosis, clearly confirming that Ly6Clow monocytes are crucial for maintaining endothelial cell homeostasis [67]. The gene discussed is APOE; the disease is atherosclerosis.