Besides functions via its receptors, estrogen also exerts protective effects against HCC by upregulating lecithin cholesterol acyltransferase (LCAT), which enhances high-density lipoprotein cholesterol (HDLC) production and uptake, thereby suppressing cholesterol biosynthesis and inhibiting tumor growth through an ESR1-dependent pathway (Figure 1D). The gene discussed is LCAT; the disease is neoplasm.