We had previously reported that ‘non-classical’ CD14+CD16+ monocytes, in contrast to ‘classical’ CD14++CD16− monocytes, are critically involved in liver fibrosis progression in humans, by perpetuating a pro-inflammatory hepatic cytokine microenvironment and directly activating collagen-producing hepatic stellate cells [4]. The gene discussed is CD14; the disease is Hepatic fibrosis.