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However, since previous in vitro studies show that the catalytic performance of PAPSS2 is 10 to 15 moments as great as that of PAPSS1,22 we speculate that PAPSS1 by itself might not provide sufficient quantities of PAPS in tissues with a high sulfation rate, such as the adrenal glands and liver. Indeed, we have proven that PAPSS2 mRNA expression in the adrenal glands and the liver is considerably higher than that of PAPSS1 expression. In addition, it’s been reported that PAPSS1 is predominantly nuclear, whereas PAPSS2 is apparently cytosolic27 predominantly; this difference in subcellular compartmentalization might explain the differential effects of PAPSS1 and PAPSS2 on cytosolic SULT2A1. In our patient, androgen excess was manifested as premature pubarche and as hirsutism later, acne, and secondary amenorrhea, therefore apparently fulfilling the existing diagnostic requirements for the polycystic ovary syndrome.1,2 However, this analysis is one of exclusion; our data show that PAPSS2 deficiency should be added to the set of defined causes of androgen excess that must be eliminated before diagnosing the polycystic ovary syndrome.