Reduced cortisol stimulates adrenocorticotrophic hormone secretion via negative feedback which then leads to adrenal hyperplasia and increased adrenal androgen production.2 These individuals also have decreased adrenal medullary function3 which has been suggested to lead to obesity and insulin resistance (IR) via the leptin pathway.4 The treatment aim in CAH is to replace the deficient hormones (glucocorticoid ± mineralocorticoid) and reduce the excessive androgens. The gene discussed is LEP; the disease is congenital adrenal hyperplasia.