The finding that heterozygous c. 402C>G FOXL2 mutation and the FOXL2 protein expression were preserved in all evaluated primary, metastatic lesions, and recurrent samples is consistent with this mutation being critical for long-term maintenance of aGCTs, as opposed to strictly tumor initiation, and may also reflect the genetically stable characteristics of aGCTs. The gene discussed is FOXL2; the disease is neoplasm.