Only one study disclosed that loss of Hsd3b7 in mice led to a complete lack of primary BAs and the accumulation of 3β,7α-dihydroxy- and 3β,7α,12α-trihydroxy-Δ(5)-cholanoic acids, the unactive forms of BAs, thereby resulting in vitamin deficiency and cholesterol malabsorption.34 The gene discussed is HSD3B7; the disease is vitamin deficiency.