The human fetus is hormonally active from an early stage in its development, with the testis and adrenal gland being major contributors of fetal steroid hormonesSteroid hormones. Following sex determination at around gestational weeks 5–6, the somatic cells of the testis begin to differentiate into hormone-producing Sertoli and Leydig cells, in parallel with the appearance of the steroidogenic cells of the fetal and definitive zones of the developing adrenal cortex, which at this stage is located close to the testis. The close association of these structures persists in humans until around 10 weeks of gestation when INSL3Insulin-like peptide 3 (INSL3) produced by the fetal Leydig cells begins to act on the gubernacular ligament to promote the first stage of testis descent to the inguinal region of the abdomen. In the first half of pregnancy, fetal hormones act more as paracrine systems diffusing locally within the fetus and amniotic fluid; consequently, understanding fetal steroidogenesis at this stage requires knowledge of both testis and adrenal metabolism. Much of fetal testis development is governed and orchestrated by feedforward and feedback processes, combining with irreversible effects, such as the involution of the Müllerian ducts, the development of the Wolffian system, and testis descent. These processes and the timing of hormone and receptor expression are what lead to the high precision that results in the extremely low frequency of non-genetic disorders of sex development. This is now being challenged by in utero low-level exposure to a range of anthropogenic chemicals, which appear capable of disrupting normal fetal development.