SRD5A2 and hyperinsulinemic hypoglycemia, familial, 4: However, we excluded the possibility of 17β‐HSD3 deficiency in our patients for the following reasons: (1) in our cohort, most patients presented normal T at baseline or after hCG stimulation, suggesting that 17β‐HSD3 enzyme activity was not absent or limited; and (2) both 17β‐HSD3 deficiency and SRD5A2 deficiency are autosomal recessive disorders, and the incidence of 17β‐HSD3 deficiency is much lower than that of 5α‐RD.