Disruption of DHEA sulfation due to inactivating mutations in the human gene encoding PAPSS2, a crucial cofactor of SULT2A1, has been shown to result in increased androgen activation and a polycystic ovary syndrome (PCOS) phenotype in both homozygous and heterozygous individuals (1, 2). The gene discussed is SULT2A1; the disease is polycystic ovary syndrome.