atypical formation of or inability to produce the first or fetal population of Leydig cells (FLCs); in mice, FLCs arise in the testicular interstitium between E12.5 and E13.0, approximately 1 day after the appearance of Sertoli cells; Sertoli cells trigger differentiation of steroidogenic factor 1-positive (SF1-positive) progenitor cells into FLCs via paracrine regulation; the intercellular Notch signaling pathway is also involved in FLC establishment and maintenance; the FLC population increases dramatically during embryonic development despite the fact that differentiating FLCs are mitotically inactive, suggesting that expansion of FLC populations results from differentiation of progenitor cells, rather than cell division of existing FLCs; the SF1-positive cells in gonadal primordia are the primary source of FLCs but other sources such as neighboring mesonephros, migrating neural crest cells, and cells from the coelomic epithelium or interstitium are potential contributors also; at the end of fetal life and during the first 2 postnatal weeks in rodents, FLCs are gradually replaced by adult Leydig cells (ALCs)