The ovary homes the oocyte reservoir, each protected and nourished by the somatic granulosa and theca cells, comprising the follicle. Folliculogenesis culminates with ovulation, a massive angiogenic response, stimulated by luteinizing hormone (LH), which leads to formation of a new endocrine gland, referred to as corpus luteum (CL). A variety of signaling molecules regulate folliculogenesis, one of which is transforming growth factor-β1 (TGFβ1). TGFβ1 is negatively regulated by Vasorin (Vasn), a transmembrane protein, shed upon cleavage to the extracellular space, trapping TGFβ1 thus attenuating its activity. Vasn, initially discovered as a component of angiogenic and tumorigenic processes, was found in our laboratory as a novel regulator of folliculogenesis. We demonstrated that Vasn expression in granulosa cells is upregulated by LH. We further established a conditional knockout (cKO) mouse model, in which Vasn is deleted specifically in granulosa cells. We showed that upon hormonal stimulation, ovulation size in Vasn cKO mice is 2-fold higher. We hypothesize that Vasn has a role in regulating the extent of the ovulatory response. This action is mediated, at least in part, by its effect on ovarian angiogenesis and may involve TGFβ1. To explore our hypothesis, we evaluated CL vasculature intravitally, employing the ovarian imaging window, developed in our laboratory. Our analysis revealed that Vasn cKO mice exhibit more vasculature then their WT siblings, possibly pointing at its antiangiogenic effect. To substantiate the involvement of Vasn-TGFβ pathway in regulating ovulation we recently established another cKO mouse, in which TGFβR2 deletion is directed to the granulosa cells.