Defective glucocorticoid signaling contributes significantly to the pathogenesis of psoriasis and arises from a broad dysregulation of the skin’s local steroidogenic machinery, including reduced expression of key enzymes (CYP11A1, CYP17, 11βHSD1, 11βHSD2), transport proteins (StAR, MLN64), and even the glucocorticoid receptor itself. The gene discussed is CYP17A1; the disease is psoriasis.