Abnormal BA will also damage the secretory function and two-way flow of the liver, and ultimately result in cholestasis.[4] The deficiency of 3β-HSD due to the mutation of HSD3B7 will result in the marked reduction or complete lack of CA and CDCA and the accumulation of hepatotoxic atypical BAs, causing reduced bile flow and subsequent malabsorption of fat-soluble vitamins as well as the progression of liver injury and cirrhosis. The gene discussed is HSD3B7; the disease is cholestasis.