The mechanism of the p.C134W FOXL2 somatic mutation to support adult-type GC tumorigenesis is under investigation (Benayoun et al. 2010; D’Angelo et al. 2011; L’Hôte et al. 2012), but the curious lack of association of this genetic variant with juvenile-type GC tumors of the ovary supports the likelihood for an alternate genetic etiology in juvenile cases. Here, FOXL2 is linked to ovarian neoplasm.