Severe fibrosis in the HF-CDAA diet model was associated with specific, profound alterations in lipid metabolism-related genes encoding both isoforms of SCD1 and SCD2 (Fig. 5) which catalyze the conversion of long-chain fatty acids into monounsaturated fatty acids, a critical step in de novo triglyceride synthesis (27). The gene discussed is SCD5; the disease is hydrops fetalis.