I enjoyed reading Prof. Findling and Prof. Raff’s recent review article on hypercortisolism (1), and this letter provides further discussion on one sentence in that article. The review states that ‘CRH-binding protein also increases during pregnancy, which may prevent the stimulatory effects of placental CRH on the maternal pituitary gland (67 (2), 68 (3), 69 (4)).’ The references cited at the end of the aforementioned statement, however, do not report that plasma levels of CRH-binding protein increase during pregnancy, and indeed, CRH-BP plasma levels decrease in the last few weeks of pregnancy so the stimulatory effects of placental CRH on the maternal pituitary gland may be increased at this time. Sasaki and coworkers wrote, ‘CRH-binding protein did not increase during pregnancy’ (3) in reference to the paper by Suda and coworkers, which reported that the amount of binding of radiolabeled CRH to CRH-BP in pregnant women’s plasma (the plasma had been stripped of endogenous CRH) does not significantly change throughout pregnancy or become significantly different from non-pregnant controls (2). When endogenous CRH was not pre-stripped from plasma, levels of radiolabeled CRH binding to the CRH-BP stayed relatively stable for the first two trimesters, and then progressively decreased to reach approximately 40% of control non-pregnant levels shortly before parturition (2). The authors concluded that, (1) rises in CRH secretion from the placenta may have been displacing the radiolabeled CRH from the CRH-BP in later pregnancy plasma samples that did not have endogenous CRH removed, (2) the assay that they used does not show actual concentrations of CRH-BP and (3) the results suggest that hypothetically, even if there was a rise in CRH-BP levels at the end of pregnancy (noting that cortisol-binding protein levels show this pattern) that their assay did not reveal, it would be small (2).