Attenuation of the promoter activation by both wt and C134W-mutated FOXL2 suggests, along with the immunoprecipitation data, that failure in the FOXL2-GATA4-SMAD3 physical and/or functional interactions with CCND2 promoter cannot fully explain how the FOXL2-C134W mutation contributes to GCT pathogenesis. Here, GATA4 is linked to granular cell tumor.