Sporadic cases of late follicular phase progesterone elevation have been described in ART cycles despite routine blockage of endogenous gonadotropins with GnRH agonists, the mechanism of which has been eluding our scrutiny. In this issue of JARG, Levran et al. report the first cases of adult-onset mild form of congenital adrenal hyperplasia (CAH) linked to a deficit in 17-hydorixyloase (17-OH ase). Contrary to CAH due to deficit 21-OH ase, these not only affect the adrenals but also the FSH driven production of E2 and androgen by the ovary thereby leading to progesterone "accumulation" during the follicular phase. Levran's findings offer new hypotheses for explaining the cases late follicular progesterone elevation particularly, when encountered in COH cycles associated with poor E2 elevation. And more importantly, Levran's findings offer new possible options for minimizing their consequences on ART outcome.