Normal development of ovarian follicles leading to ovulation depends on interactions between the oocyte and somatic cells in the follicle as well as the general physiological milieu. The oocyte-secreted molecules bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9) are essential for normal ovarian follicle growth and function (Shimisaki et al. 2003). Mutations in both BMP15 (FecXG) and GDF9 (FecGH) have been shown to be segregating in the Cambridge breed and ewes that are heterozygous carriers of either of these mutations have greatly increased ovulation rate while homozygous carriers of either mutation are sterile with a typical ovarian hypoplasia (Hanrahan et al. 2004). The sterility is due to failure of follicular development to progress beyond the primary follicle stage. However, not all cases of ovarian hypoplasia in Cambridge ewes could be explained by these mutations and sequencing of the entire coding regions for these genes did not reveal any mutations that could account for their typical sterile phenotype (Hanrahan et al. 2004). It was suggested, based on pedigree analysis of the four ‘unexplained’ sterile ewes, that another gene was responsible. The present report concerns the available evidence concerning this hypothesis.