SUMMARY Cryptorchidism occurs in about 1% of boys, but has a raised incidence in those with deficiencies of androgen function. Greater knowledge of fetal‐maternal endocrinology and related experimental work has provided evidence that fetal testicular endocrine function is vital in descent of the gonad. The therapeutic use of hCG has, however, been disappointing, and its role is confined to helping to distinguish the retractile from the undescended testis. Cryptorchidism is commonly associated with congenital pathological defects such as ductal abnormalities, and others (including interstitial fibrosis and a reduction in germ cells) develop after 1‐2 years, while later these patients are at greater risk of carcinoma in situ and germ cell cancer. The demonstration of the early pathological changes has recently dictated much earlier surgical correction, but long‐term follow‐up is needed to prove clinical benefit from this practice.