It is well established in various experimental models that luteinizing hormone (LH) stimulated testosterone (T) production of Leydig cells is the key endocrine stimulus of spermatogenesis. The role of the other gonadotrophin, follicle-stimulating hormone (FSH), is as yet somewhat unclear given that several clinical conditions and experimental models, including men with inactivating FSH receptor (R) mutation and male Fshb and Fshrknockout mice, maintain fairly normal spermatogenesis and fertility. Furthermore, FSH treatment of male infertility has produced at best modest results. On the other hand, there are animal species (e.g. teleost fishes and the Djungarian hamster) where spermatogenesis is primarily FSH-dependent. The purpose of this article is to briefly review the gonadotrophin dependence of spermatogenesis in several model species and examine how it has shifted during evolution from FSH to LH dominance. The information may provide new insight into the role of FSH treatment of male infertility.