The near universal presence of this FOXL2 mutation in adult-type granulosa cell tumors, the fact that most tumors are hemizygous for the mutation, and the presence of abundant FOXL2 protein in tumor cell nuclei (Figure 3) suggest that this mutation is a critical genetic abnormality in the genesis of adult-type granulosa cell tumors and that it is an activating mutation. Here, FOXL2 is linked to granulosa cell tumor.