All ovarian follicles are doomed to degenerate through atresia unless they receive adequate trophic support from specific growth-differentiation factors or gonadotrophins at critical stages in their development. Throughout folliculogenesis, granulosa cells strongly express transforming growth factor-beta (TGFβ) superfamily genes encoding homo- or heterodimeric proteins that orchestrate the entire process of oogenesis at autocrine and paracrine levels. It is clearly established that ovarian ageing is heritable in women. The development-related changes in TGF�uperfamily gene expression throughout folliculogenesis create an efflux of potential biomarkers in blood or urine that can be measured to reflect follicle number and stage of maturity. Such assays potentially provide a rational basis for the endocrine diagnosis of ovarian sufficiency, in combination with conventional markers of ovarian status (follicle-stimulating hormone and estradiol) and ultrasonographic measurements of follicle size and number. Unquestionably, human homologues of the numerous mouse genes that regulate ovarian ageing operate in women.