When administered without glucocorticoids, abiraterone acetate induces a syndrome of secondary mineralocorticoid excess due to CYP17A1 17α-hydroxylase inhibition, consequently decreased glucocorticoid production, and a compensatory increase in adrenocorticotrophic hormone (ACTH), resulting in a rise in steroids with mineralocorticoid properties upstream of CYP17A1.5,6 In addition to maximizing efficacy for treating prostate cancer, glucocorticoids are combined with abiraterone acetate to prevent this syndrome; however, glucocorticoid exposure may exceed physiological requirements. This evidence concerns the gene CYP17A1 and prostate carcinoma.