Studies from mouse models have shown that defects in PGC migration or proliferation (e.g. Steel, c-kit, Cxcr4) can be associated with subsequent ovarian germ cell depletion and ovarian insufficiency in postnatal or adult life (Edson et al., 2009; Jagarlamudi et al., 2010). Here, CXCR4 is linked to ovarian dysfunction.